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1.
Int. j. morphol ; 38(3): 523-529, June 2020. graf
Article in English | LILACS | ID: biblio-1098282

ABSTRACT

This study aimed to investigate the morphometric and the pattern of protein and gene expression related to the extrinsic apoptotic pathway in experimental focal cerebral ischemia and the hole of neuroprotection with hypothermia and ketoprofen. For this analysis, 120 rats were randomly divided into 3 groups (20 animals each): control - no surgery (20 animals); sham - simulation of surgery (20 animals); ischemic - focal ischemia for 1 hour, without reperfusion (80 animals) and divided into four subgroups with 20 animals each: ischemic + intraischemic hypothermia; ischemic + previous intravenous ketoprofen, and ischemic + hypothermia and ketoprofen. The infarct volume was measured using morphometric analysis of infarct areas defined by triphenyl tetrazolium chloride and the patterns of expression of the apoptosis genes (Fas, c-Flip, caspase-8 and caspase-3) and the apoptosis protein caspase-3 were evaluated by quantitative real-time PCR and immunohistochemistry, respectively. Hypo expression of genes of extrinsic pathway of apoptosis was observed: Fas receptor, c-Flip and caspase-8 in the ischemics areas. Increases in the gene and protein caspase-3 in the ischemic areas were also observed, and these increases were reduced by hypothermia and ketoprofen, also noted in the morphometric study. The caspases-3 increase suggests that this gene plays an important role in apoptosis, probably culminating in cell death and that the neuroprotective effect of hypothermia and ketoprofen is involved.


Este estudio tuvo como objetivo investigar la morfometría y el patrón de expresión de proteínas y genes relacionados con la vía apoptótica extrínseca en la isquemia cerebral focal experimental y el agujero de neuroprotección con hipotermia y ketoprofeno. Se dividieron aleatoriamente 120 ratas en 3 grupos (20 animales cada uno): control - sin cirugía (20 animales); simulación - simulación de cirugía (20 animales); isquemia isquemia focal durante 1 hora, sin reperfusión (80 animales) y dividida en cuatro subgrupos con 20 animales cada uno: isquemia + hipotermia intraisquémica; isquemia + ketoprofeno intravenoso previo, e isquemia + hipotermia y ketoprofeno. El volumen del infarto se midió utilizando un análisis morfométrico de áreas de infarto definidas por cloruro de trifenil tetrazolio y los patrones de expresión de los genes de apoptosis (Fas, c-Flip, caspase-8 y caspase-3) y la proteína de apoptosis caspase-3 fueron evaluados por PCR cuantitativa en tiempo real e inmunohistoquímica, respectivamente. Se observó hipoexpresión de genes de la vía extrínseca de la apoptosis: receptor Fas, c-Flip y caspasa-8 en las áreas isquémicas. También se observaron aumentos en el gen y la proteína caspasa-3 en las áreas isquémicas y estos aumentos se redujeron por hipotermia y ketoprofeno, también observado por estudio morfométrico. El aumento de caspasas-3 sugiere que este gen tiene un papel importante en la apoptosis, y probable causa de muerte celular, involucrando el efecto neuroprotector de la hipotermia y el ketoprofeno.


Subject(s)
Animals , Rats , Brain Ischemia/genetics , Brain Ischemia/metabolism , Immunohistochemistry , Brain Ischemia/pathology , Brain Ischemia/therapy , Ketoprofen/pharmacology , Apoptosis/genetics , Neuroprotective Agents/pharmacology , Disease Models, Animal , Caspase 3/genetics , Caspase 8/genetics , Real-Time Polymerase Chain Reaction , Hypothermia, Induced
2.
Rev. chil. neuropsicol. (En línea) ; 14(2): 35-39, dic. 2019. ilus
Article in Spanish | LILACS | ID: biblio-1102455

ABSTRACT

La isquemia cerebral es el tipo de accidente cerebrovascular más común, generando altas tasas de mortalidad y morbilidad a nivel mundial. El entendimiento de la fisiopatología de la lesión cerebral ha requerido de la implementación de modelos experimentales que permitan evaluar los fenómenos celulares, sobre todo aquellos a largo plazo. Por tal razón, el objetivo del presente trabajo fue evaluar las áreas exofocales a un mes y cuatro meses post-isquemia cerebral en un modelo experimental. Ratas Wistar fueron sometidas a una isquemia focal transitoria (t-MCAo) y un grupo fueron sacrificados al mes y otro grupo a los cuatro meses post-isquemia para su posterior análisis histológico. Los cortes fueron teñidos con Nissl y se realizó inmunohistoquímica de la proteína Tau. Nuestros resultados muestran tres áreas de lesión exofocal tanto al mes como a los cuatro meses post-isquemia: el giro dentado, la amígdala y el tálamo. Estas regiones se han asociado al control emocional, lo cual sugiere que a largo término post-isquemia se tengan en cuenta hallazgos clínicos que evalúen cambios emocionales en los pacientes que han sufrido un evento isquémico cerebral.


Cerebral ischemia is the most common type of stroke, which generates high mortality and morbidity rates worldwide. The understanding of the pathophysiology of brain injury has required the implementation of experimental models that allow the evaluation of cellular phenomena, especially those in the long-term. For this reason, the objective of the present work was to evaluate the exofocal areas at one month and four months after cerebral ischemia. Wistar rats were subjected to transient focal ischemia (t-MCAo) and one group was sacrificed one month and another group at four months' post-ischemia for subsequent histological analysis. The cuts were stained with Nissl and immunohistochemistry of the Tau protein was performed. Our results show three areas of exofocal lesion both one month and four months' post-ischemia: the thalamus, the dentate gyrus, and the amygdala. These regions have been associated with emotional control, which suggests that in the long-term post-ischemia clinical findings that evaluate emotional changes in patients who have suffered a cerebral ischemic event should be considered.


Subject(s)
Animals , Rats , Thalamus/pathology , Brain Ischemia/pathology , Dentate Gyrus/pathology , Amygdala/pathology , Immunohistochemistry , Disease Models, Animal
3.
Arq. neuropsiquiatr ; 77(10): 689-695, Oct. 2019. graf
Article in English | LILACS | ID: biblio-1038728

ABSTRACT

ABSTRACT This study aimed to analyze the cerebellum of rats submitted to an experimental focal cerebral ischemia, by middle cerebral artery occlusion for 90 minutes, followed by reperfusion for 48 hours, associated with an alcoholism model. Methods Fifty adult Wistar rats were used, subdivided into five experimental groups: control group (C): animals submitted to anesthesia only; sham group (S): animals submitted to complete simulation of the surgical procedure; ischemic group (I): animals submitted to focal cerebral ischemia for 90 minutes followed by reperfusion for 48 hours; alcoholic group (A): animals that received daily absolute ethanol diluted 20% in water for four weeks; and, ischemic and alcoholic group (I + A): animals receiving the same treatment as group A and, after four weeks, submitted to focal cerebral ischemia for 90 minutes, followed by reperfusion for 48 hours. The cerebellum samples were collected and immunohistochemical analysis of Caspase-9 protein and serum analysis by RT-PCR of microRNAs miR-21, miR-126 and miR155 were performed. Results The expression of Caspase-9 was higher in groups I, A and I + A. In the microRNAs analyses, miR-126 was higher in groups A and I + A, miR-155 was higher in groups I and I + A. Conclusions We conclude that apoptosis occurs in the cerebellar cortex, even if it is distant from the ischemic focus, and that microRNAs 126 and 155 show a correlation with cellular apoptosis in ischemic rats and those submitted to the chronic alcohol model.


RESUMO O objetivo deste estudo foi analisar o cerebelo de ratos submetidos à isquemia cerebral focal experimental, por oclusão da artéria cerebral média por 90 minutos, seguida de reperfusão por 48 horas, associada a um modelo de alcoolismo. Métodos Foram utilizados 50 ratos Wistar adultos, subdivididos em cinco grupos experimentais: grupo controle (C): animais submetidos apenas à anestesia; grupo sham (S): animais submetidos à simulação completa do procedimento cirúrgico; grupo isquêmico (I): animais submetidos à isquemia cerebral focal por 90 minutos, seguidos de reperfusão por 48 horas; grupo alcoólico (A): animais que receberam etanol absoluto diário diluído em 20% em água por quatro semanas; e grupo isquêmico e alcoólico (I + A): animais que recebem o mesmo tratamento do grupo A e, após quatro semanas, submetidos à isquemia cerebral focal por 90 minutos, seguidos de reperfusão por 48 horas. As amostras de cerebelo foram coletadas e a análise imuno-histoquímica da proteína Caspase-9 e a análise sérica por RT-PCR dos microRNAs miR-21, miR-126 e miR155 foram realizadas. Resultados A expressão de Caspase-9 foi maior nos grupos I, A e I + A. Nas análises de microRNAs, o miR-126 foi maior nos grupos A e I + A, o miR-155 foi maior nos grupos I e I + A. Conclusões Concluímos que a apoptose ocorre no córtex cerebelar, mesmo distante do foco isquêmico, e que os microRNAs 126 e 155 mostram uma correlação com a apoptose celular em ratos isquêmicos e submetidos ao modelo crônico de álcool.


Subject(s)
Animals , Male , Cerebellum/pathology , Brain Ischemia/pathology , Apoptosis , MicroRNAs/blood , Alcoholism/pathology , Caspase 9/analysis , Time Factors , Immunohistochemistry , Reperfusion Injury/pathology , Random Allocation , Cerebellum/chemistry , Brain Ischemia/blood , Rats, Wistar , Infarction, Middle Cerebral Artery , Alcoholism/blood , Real-Time Polymerase Chain Reaction
4.
Medicina (B.Aires) ; 79(1): 61-63, feb. 2019. ilus
Article in Spanish | LILACS | ID: biblio-1002588

ABSTRACT

La endocarditis trombótica no bacteriana, antiguamente conocida como endocarditis marántica, es una entidad infrecuente en la que se desarrollan vegetaciones estériles, compuestas por fibrina en las válvulas del corazón. Suele diagnosticarse en el momento de la autopsia o en enfermedades oncológicas avanzadas. Las neoplasias malignas más frecuentemente asociadas con esta entidad son las de pulmón, páncreas, estómago y adenocarcinomas de origen primario desconocido. Es necesario descartar la endocarditis infecciosa y establecer la presencia de vegetaciones valvulares mediante ecocardiografía. Presentamos el caso de una paciente con diagnóstico reciente de adenocarcinoma de estómago en estadio avanzado que presentó ceguera cortical e imágenes compatibles con isquemia cerebral. El ecocardiograma transesofágico mostró dos vegetaciones en válvula mitral. Los hemocultivos fueron negativos. Se enfatiza la importancia de sospechar endocarditis trombótica no bacteriana en enfermos con cáncer y embolismo sistémico.


Nonbacterial thrombotic endocarditis, formerly known as marantic endocarditis, it is an infrequent entity in which sterile, fibrin vegetations develop on heart valve leaflets. It is often diagnosed at the time of autopsy or in late-stage malignancies. The most common malignancies associated with nonbacterial thrombotic endocarditis are lung, pancreatic, gastric cancer and adenocarcinomas of an unknown primary site. Diagnosis requires ruling out infective endocarditis and establishing the presence of valvular vegetations using echocardiography. We report the case of a patient with a recent diagnosis of advanced gastric adenocarcinoma who presented with cortical blindness. The computed tomography was compatible with cerebral ischemia. The transoesophageal echocardiogram showed two vegetations in mitral valve. Blood cultures were negative. We emphasize the importance of suspecting nonbacterial thrombotic endocarditis in patients with cancer and systemic embolism.


Subject(s)
Humans , Female , Aged , Blindness, Cortical/etiology , Endocarditis, Non-Infective/complications , Stomach Neoplasms/complications , Adenocarcinoma/complications , Tomography, X-Ray Computed/methods , Brain Ischemia/complications , Brain Ischemia/pathology , Brain Ischemia/diagnostic imaging , Blindness, Cortical/pathology , Blindness, Cortical/diagnostic imaging , Endocarditis, Non-Infective/pathology
5.
Rev. méd. Chile ; 146(11): 1356-1360, nov. 2018. graf
Article in Spanish | LILACS | ID: biblio-985711

ABSTRACT

Giant cell arteritis is the most common vasculitis in patients aged over 50 years. We report an 89-year-old woman with significant weight loss and persistent frontal-occipital headaches lasting two months. The neurological examination at admission identified a decrease in visual acuity of the left eye, paralysis of the third cranial nerve of the right eye and alterations of body motility without objective signs of damage of the motor or sensitive pathways. Magnetic resonance imaging showed changes of the temporal artery wall and in both vertebral arteries, as well as bilateral cerebellar and occipital ischemic lesions. The Doppler ultrasound of the temporal arteries was compatible with Giant cell arteritis. Treatment with steroids was started. While receiving oral prednisone, the patient suffered new infarcts of the posterior territory, documented with a CAT scan.


Subject(s)
Humans , Female , Aged, 80 and over , Giant Cell Arteritis/diagnostic imaging , Basilar Artery/diagnostic imaging , Vertebral Artery/diagnostic imaging , Oculomotor Nerve Diseases/diagnostic imaging , Brain Ischemia/diagnostic imaging , Oculomotor Nerve/diagnostic imaging , Temporal Arteries/diagnostic imaging , Giant Cell Arteritis/etiology , Giant Cell Arteritis/pathology , Basilar Artery/pathology , Vertebral Artery/pathology , Magnetic Resonance Imaging/methods , Oculomotor Nerve Diseases/etiology , Oculomotor Nerve Diseases/pathology , Brain Ischemia/etiology , Brain Ischemia/pathology , Ultrasonography, Doppler/methods , Oculomotor Nerve/pathology
6.
Arq. neuropsiquiatr ; 75(10): 692-696, Oct. 2017. tab
Article in English | LILACS | ID: biblio-888256

ABSTRACT

ABSTRACT Objective: To explore the influence of infarct location on long-term functional outcome following a first-ever arterial ischemic stroke (AIS) in non-neonate children. Method: The MRIs of 39 children with AIS (median age 5.38 years; 36% girls; mean follow-up time 5.87 years) were prospectively evaluated. Infarct location was classified as the absence or presence of subcortical involvement. Functional outcome was measured using the modified Rankin scale (mRS) for children after the follow-up assessment. We utilized multivariate logistic regression models to estimate the odds ratios (ORs) for the outcome while adjusting for age, sex, infarct size and middle cerebral artery territory involvement (significance < 0.05). Results: Both infarcts ≥ 4% of total brain volume (OR 9.92; CI 1.76 - 55.9; p 0.009) and the presence of subcortical involvement (OR 8.36; CI 1.76 - 53.6; p 0.025) independently increased the risk of marked functional impairment (mRS 3 to 5). Conclusion: Infarct extension and location can help predict the extent of disability after childhood AIS.


RESUMEN Objetivo: Para explorar la influencia de la localización del infarto sobre los resultados funcionales a largo plazo después de un primer ictus isquémico arterial (IIA) en ninos posterior a la edad neonatal. Métodos: Se evaluaron de forma prospectiva imágenes por RM de 39 ninos con IIA (mediana de edad: 5,38 años; 36% ninas; seguimiento promedio: 5,87 anos). La localización del infarto fue clasificada como ausencia o presencia de compromiso subcortical. El resultado funcional fue medido utilizando la escala modificada de Rankin (mRS) para ninos en una evaluación al final del seguimiento. Utilizamos modelos de regresión logística multivariada para estimar los odds ratios (ORs) para el resultado ajustado para la edad, sexo, tamaño del infarto y compromiso del territorio vascular de la arteria cerebral media (significancia < 0,05). Resultados: Tanto el tamaño del infarto > 4% del volumen encefálico total (OR 9,92; IC 1,76-55,9; p 0,009) como la presencia de compromiso subcortical (OR 8,36; IC 1,76-53,6; p 0,025) incrementaron independientemente el riesgo de presentar marcado compromiso funcional (mRS 3 a 5). Conclusión: La extensión y localización del infarto pueden ayudar a predecir la magnitud de la discapacidad posterior a un IIA durante la niñez.


Subject(s)
Humans , Male , Female , Infant , Child, Preschool , Child , Brain Ischemia/pathology , Stroke/pathology , Prognosis , Magnetic Resonance Imaging , Brain Ischemia/diagnostic imaging , Prospective Studies , Recovery of Function , Stroke/diagnostic imaging , Disability Evaluation
7.
Rev. bras. anestesiol ; 66(6): 583-593, Nov.-Dec. 2016. tab, graf
Article in English | LILACS | ID: biblio-829717

ABSTRACT

Abstract This study was designed to investigate whether dexmedetomidine and thiopental have cerebral protective effects after focal cerebral ischemia in rats. Thirty male Sprague Dawley rats were randomly assigned to three groups: control group (Group C, n = 10), dexmedetomidine group (Group D, n = 10), thiopental group (Group T, n = 10). After all rats were anesthetized, they were intubated, then mechanically ventilated. A catheter was inserted into the right femoral artery for continuous mean arterial pressure, physiological parameters and blood sampling at baseline, 5 min after occlusion and 20 min after reperfusion. A catheter was inserted into the left femoral vein for intravenous (IV) medication administration. Right common carotid artery of each rat was isolated and clamped for 45 min. At the end of the duration common carotid artery were unclamped and the brain reperfusion was achieved for 90 min. Dexmedetomidine was administered for Group D IV infusion, and Group T received thiopental IV. According to histopathologic scores cerebral ischemia was documented in all rats in Group C, but no ischemia was found in three rats in Group T and in four rats in Group D. Grade 3 cerebral ischemia was documented in three rats in Group C, and in only one rat in both groups T and D. For histopathologic grades the difference between Group T and Group D was not significant (p > 0.05). But the differences between Group C and Group T (p < 0.05) and Group C and Group D (p < 0.01) were statically significant. In conclusion, we demonstrated that dexmedetomidine and thiopental have experimental histopathologic cerebral protective effects on experimental focal cerebral ischemia in rats.


Resumo Este estudo foi desenhado para investigar se dexmedetomidina e tiopental têm efeitos protetores cerebrais após isquemia cerebral focal em ratos. Trinta ratos da linhagem Sprague Dawley foram randomicamente alocados em três grupos: controle (Grupo C, n = 10), dexmedetomidina (Grupo D, n = 10) e tiopental (Grupo T, n = 10). Após a anestesia, foram intubados e ventilados mecanicamente. Um cateter foi inserido na artéria femoral direita para monitoração contínua da pressão arterial média (PAM) e dos parâmetros fisiológicos e para coleta de amostras de sangue na fase basal, 5 minutos após a oclusão e 20 minutos após a reperfusão. Um cateter foi inserido na veia femoral esquerda para administração intravenosa (IV) de medicamentos. A artéria carótida comum direita de cada rato foi isolada e pinçada durante 45 minutos. No fim dos 45 minutos, o pinçamento foi removido e a reperfusão do cérebro foi obtida por 90 minutos. Dexmedetomidina foi administrada por infusão IV no Grupo D e tiopental no Grupo T. De acordo com as pontuações histopatológicas, isquemia cerebral foi observada em todos os ratos do Grupo C, mas não foi encontrada em três ratos do Grupo T e em quatro ratos do Grupo D. O grau 3 de isquemia cerebral foi encontrada em três ratos do grupo C e em apenas um rato de ambos os grupos T e D. Para os graus histopatológicos, a diferença entre o Grupo T e o Grupo D não foi significativa (p > 0,05). Porém, as diferenças entre o Grupo C e o Grupo T (p < 0,05) e entre o Grupo C e o Grupo D (p < 0,01) foram estatisticamente significativas. Em conclusão, demonstramos que dexmedetomidina e tiopental têm efeitos histopatológicos protetores cerebrais sobre isquemia cerebral focal experimental em ratos.


Subject(s)
Animals , Male , Rats , Thiopental/therapeutic use , Brain Ischemia/prevention & control , Neuroprotective Agents/therapeutic use , Dexmedetomidine/therapeutic use , Hypnotics and Sedatives/therapeutic use , Respiration, Artificial , Reperfusion Injury/prevention & control , Brain Ischemia/pathology , Rats, Sprague-Dawley , Anesthesia
8.
Rev. bras. anestesiol ; 66(6): 613-621, Nov.-Dec. 2016. tab, graf
Article in English | LILACS | ID: biblio-829707

ABSTRACT

Abstract Background and objectives: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. Methods: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. Results: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. Conclusions: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.


Resumo Justificativa e objetivos: Isoflurano é um éter volátil halogenado usado para anestesia por via inalatória. É amplamente usado na clínica como um anestésico para inalação. A lesão hipóxico-isquêmica neonatal ocorre no cérebro imaturo e resulta em morte celular tardia via excitotoxicidade e estresse oxidativo. Isoflurano mostrou ter propriedades neuroprotetoras que formam uma base benéfica para o seu uso tanto em cultura de células quanto em modelos animais, incluindo vários modelos de lesão cerebral. Nosso objetivo foi determinar o efeito neuroprotetor de isoflurano em hipóxia cerebral e elucidar o mecanismo subjacente. Métodos: Fatias de hipocampo, em fluido cerebrospinal artificial (CSFA) com glicose e privação de oxigênio, foram usadas como um modelo in vitro de hipóxia cerebral. O pico de população ortodrômica (PPO) e o potencial de lesão hipóxica (PLH) foram registrados nas regiões CA1 e CA3. A concentração de neurotransmissores de aminoácidos na solução de perfusão das fatias de hipocampo foi medida. Resultados: O tratamento com isoflurano retardou a eliminação do PPO e melhorou a recuperação do PPO; diminuiu a frequência do PLH, retardou o início do PLH e aumentou a duração do PLH. O tratamento com isoflurano também diminuiu a liberação de neurotransmissores de aminoácidos induzida pela hipóxia, como aspartato, glutamato e glicina, mas os níveis de ácido γ-aminobutírico (GABA) estavam elevados. Estudos morfológicos mostram que o tratamento de edema com isoflurano atenuou o edema de neurônios piramidais na região CA1. Também reduziu a apoptose, como mostrado pela expressão reduzida da caspase-3 e genes PARP. Conclusões: Isoflurano mostrou um efeito neuroprotetor na lesão neuronal no hipocampo induzida por hipóxia através da supressão de apoptose.


Subject(s)
Animals , Female , Pregnancy , Rats , Hypoxia, Brain/prevention & control , Brain Ischemia/pathology , Apoptosis/drug effects , Neuroprotective Agents/pharmacology , Anesthetics, Inhalation/pharmacology , Isoflurane/pharmacology , Hypoxia, Brain/pathology , Rats, Sprague-Dawley , CA1 Region, Hippocampal/pathology , CA3 Region, Hippocampal/pathology , Glucose/deficiency , Hippocampus/pathology , Animals, Newborn
9.
Acta cir. bras ; 31(9): 629-637, Sept. 2016. graf
Article in English | LILACS | ID: lil-795996

ABSTRACT

ABSTRACT PURPOSE: To evaluated histopathological changes, morphometric and expression of proteins CASPASE-3, BCL-2 and XIAP related to apoptosis in the cerebellum after induction of temporary focal cerebral ischemia followed by reperfusion, with or without a model of chronic alcoholism. METHODS: Fifty Wistar rats were used and divided into: control group (C), sham group (S), ischemic group (I), alcoholic group (A), and ischemic and alcoholic group (IA). The cerebellum samples collected were stained for histopathological and morphometric analysis and immunohistochemistry study. RESULTS: Histopathological changes were observed a greater degree in animals in groups A and IA. The morphometric study showed no difference in the amount of cells in the granular layer of the cerebellum between the groups. The expression of CASPASE-3 was higher than BCL-2 and XIAP in the groups A and IA. CONCLUSION: We observed correlation between histopathological changes and the occurrence of apoptosis in cerebellar cortex.


Subject(s)
Animals , Male , Cerebellum/pathology , Brain Ischemia/pathology , Apoptosis , Ethanol/pharmacology , Alcoholism/pathology , Apoptosis Regulatory Proteins/metabolism , Immunohistochemistry , Reperfusion Injury/pathology , Cerebellum/drug effects , Cerebellum/metabolism , Brain Ischemia/metabolism , Rats, Wistar , Statistics, Nonparametric , Proto-Oncogene Proteins c-bcl-2/metabolism , Disease Models, Animal , Alcoholism/metabolism , X-Linked Inhibitor of Apoptosis Protein/metabolism , Caspase 3/metabolism
10.
Arq. neuropsiquiatr ; 73(5): 408-414, 05/2015. tab, graf
Article in English | LILACS | ID: lil-746490

ABSTRACT

Objective The potential of computed tomography angiography (CTA) was assessed for early determination of stroke subtypes in a Brazilian cohort of patients with stroke. Method From July 2011 to July 2013, we selected patients with suspected hyperacute stroke (< 6 hours). Intracranial and cervical arteries were scrutinized on CTA and their imaging features were correlated with concurrent subtype of stroke. Results Stroke was documented in 50/106 selected patients (47.2%) based on both clinical grounds and imaging follow-up (stroke group), with statistically significant arterial stenosis and vulnerable plaques on CTA. Intracranial large artery disease was demonstrated in 34% of patients in the stroke group. Partial territorial infarct prevailed (86%) while artery-to-artery embolization was the most common stroke mechanism (52%). Conclusion Multidetector CTA was useful for the etiologic work-up of hyperacute ischemic stroke and facilitated the knowledge about the topographic pattern of brain infarct in accordance with its causative mechanism. .


Objetivo Avaliar o potencial da angiotomografia computadorizada multidetectores (ATCM) na determinação etiológica precoce do acidente vascular encefálico (AVE) e correlacionar o mecanismo causal com o padrão de infarto. Método De Julho de 2011 a Julho de 2013, foram selecionados os pacientes com suspeita clínica de AVE hiperagudo. Os achados da ATCM dos vasos intracranianos e cervicais foram correlacionados com a etiologia final do evento. Resultados AVE foi confirmado em 50/106 pacientes (47,2%). Estes apresentaram alterações angiográficas estatisticamente mais relevantes. Aterosclerose dos grandes vasos intracranianos esteve presente em 34% destes pacientes. O padrão radiológico topográfico de infarto mais comum foi o infarto territorial parcial (86%). A embolização arterio-arterial foi o mecanismo mais prevalente (52%). Conclusão A utilização da ATCM traz benefícios na detecção etiológica precoce dos pacientes com suspeita de AVE hiperagudo, além de possibilitar o entendimento do padrão radiológico topográfico de acordo com o mecanismo causal do evento isquêmico. .


Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Brain Infarction/etiology , Brain Infarction , Brain Ischemia/etiology , Brain Ischemia , Cerebral Angiography/methods , Multidetector Computed Tomography/methods , Acute Disease , Brazil , Brain Infarction/pathology , Brain Ischemia/pathology , Early Diagnosis , Intracranial Arteriosclerosis/complications , Intracranial Arteriosclerosis , Retrospective Studies , Time Factors
11.
Mem. Inst. Oswaldo Cruz ; 110(2): 181-191, 04/2015. graf
Article in English | LILACS | ID: lil-744476

ABSTRACT

Chagas disease, caused by the intracellular protozoan Trypanosoma cruzi, is a serious health problem in Latin America. During this parasitic infection, the heart is one of the major organs affected. The pathogenesis of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection and the molecular mechanisms that occur immediately following parasite entry into host cells are not yet completely understood. When cells are infected with T. cruzi, they develop an inflammatory response, in which cyclooxygenase-2 (COX-2) catalyses rate-limiting steps in the arachidonic acid pathway. However, how the parasite interaction modulates COX-2 activity is poorly understood. In this study, the H9c2 cell line was used as our model and we investigated cellular and biochemical aspects during the initial 48 h of parasitic infection. Oscillatory activity of COX-2 was observed, which correlated with the control of the pro-inflammatory environment in infected cells. Interestingly, subcellular trafficking was also verified, correlated with the control of Cox-2 mRNA or the activated COX-2 protein in cells, which is directly connected with the assemble of stress granules structures. Our collective findings suggest that in the very early stage of the T. cruzi-host cell interaction, the parasite is able to modulate the cellular metabolism in order to survives.


Subject(s)
Humans , Brain Ischemia/pathology , Brain/pathology , Neuroimaging/methods , Stroke/pathology , Chronic Disease
12.
Biomédica (Bogotá) ; 34(3): 366-378, July-Sept. 2014. ilus
Article in Spanish | LILACS | ID: lil-726786

ABSTRACT

Introducción. El accidente cerebrovascular es la segunda causa de muerte y la primera de discapacidad en el mundo, y más de 85 % es de origen isquémico. Objetivo. Evaluar en un modelo de infarto cerebral por embolia arterial el efecto de la atorvastatina y el meloxicam, administrados por separado y de forma conjunta, sobre la respuesta neuronal, los astrocitos y la microglia. Materiales y métodos. Se sometieron ratas Wistar a embolia de la arteria carótida y a tratamiento con meloxicam y atorvastatina, administrados por separado y conjuntamente, a las 6, 24, 48 y 72 horas. Se evaluó la reacción de las proteínas COX-2, GFAP y OX-42 en las neuronas, los astrocitos y la microglia mediante inmunohistoquímica y estudios morfológicos y de densitometría. Los datos obtenidos se evaluaron por medio de un análisis de varianza y de pruebas no paramétricas de comparación múltiple. Resultados. La isquemia cerebral por embolia arterial incrementó significativamente (p<0,001) la reacción de los astrocitos y la microglia, en tanto que la atorvastatina y el meloxicam, administrados por separado y de forma conjunta, la redujeron. La isquemia produjo acortamiento de las proyecciones de los astrocitos, engrosamiento celular, ruptura de las expansiones protoplásmicas (clasmatodendrosis) y cambios morfológicos en la microglia propios de diversas etapas de actividad. En las zonas circundantes del foco se incrementó la reacción inmunológica de la COX-2 y se redujo en el foco isquémico, en tanto que el meloxicam y la atorvastatina redujeron significativamente (p<0,001) la reacción inmunológica en la zona circundante del foco, restableciendo la marcación de la ciclooxigenasa en el foco isquémico. Conclusión. La combinación de meloxicam y atorvastatina atenúa la respuesta de los astrocitos y la microglia en el proceso inflamatorio posterior a la isquemia cerebral por embolia arterial, reduciendo la degeneración neuronal y restableciendo el equilibrio morfológico y funcional del tejido nervioso.


Introduction: Stroke is the second leading cause of death and the first cause of disability in the world, with more than 85% of the cases having ischemic origin. Objective: To evaluate in an embolism model of stroke the effect of atorvastatin and meloxicam on neurons, astrocytes and microglia. This evaluation was done administering each medication individually and in association. Materials and methods: Wistar rats were subjected to carotid arterial embolism and treatment with meloxicam and atorvastatin at 6, 24, 48 and 72 hours. Using immunohistochemistry, we evaluated the immunoreactivity of COX-2 protein, GFAP and OX-42 in neurons, astrocytes and microglia by densitometric and morphological studies. Data were evaluated by variance analysis and non-parametric multiple comparison. Results: Cerebral ischemia by arterial embolism increased significantly the reactivity of microglia and astrocytes (p<0.001), whereas it was reduced by atorvastatin, meloxicam and their association. Ischemia produced astrocytic shortening, cellular thickening, protoplasmic rupture expansions (clasmatodendrosis) and microglial morphological changes characteristic of various activity stages. In perifocal areas, immunoreactivity of COX-2 was increased and in the ischemic focus it was reduced, while meloxicam and atorvastatin significantly reduced (p<0.001) perifocal immunoreactivity, restoring the marking of cyclooxygenase in the ischemic focus. Conclusion: These results suggest that the meloxicam-atorvastatin association attenuates astrocytic and microglial response in the inflammatory process after cerebral ischemia by arterial embolism, reducing neurodegeneration and restoring the morphological and functional balance of nervous tissue .


Subject(s)
Animals , Female , Rats , Brain Ischemia/drug therapy , Cyclooxygenase Inhibitors/therapeutic use , Heptanoic Acids/therapeutic use , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Intracranial Embolism/complications , Nerve Degeneration/prevention & control , Pyrroles/therapeutic use , Thiazines/therapeutic use , Thiazoles/therapeutic use , Atorvastatin , /analysis , Astrocytes/drug effects , Astrocytes/pathology , Biomarkers , Brain Ischemia/etiology , Brain Ischemia/pathology , Carotid Stenosis/complications , Carotid Stenosis/pathology , Cyclooxygenase Inhibitors/administration & dosage , Disease Models, Animal , Drug Evaluation, Preclinical , Glial Fibrillary Acidic Protein/analysis , Heptanoic Acids/administration & dosage , Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage , Inflammation , Intracranial Embolism/pathology , Microglia/drug effects , Microglia/pathology , Nerve Tissue Proteins/analysis , Pyrroles/administration & dosage , Random Allocation , Rats, Wistar , Thiazines/administration & dosage , Thiazoles/administration & dosage
13.
Int. j. morphol ; 30(3): 979-985, Sept. 2012. ilus
Article in English | LILACS | ID: lil-665512

ABSTRACT

NMDAR (N-methyl-D-aspartate receptor) is one subtype of ionotrophic glutamate receptor which is extensively distributed in the central nervous system (CNS). In the mammalian CNS, NMDAR serves prominent roles in the pathophysiologic process of cerebral ischemia. This study aimed to investigate the pattern of expression of protein and gene of the excitatory neurotransmitter NMDAR in experimental focal cerebral ischemia and the hole of neuroprotection with hypothermia and ketoprofen. 120 rats were randomly divided into 6 groups (20 animals each): control - no surgery; sham - simulation of surgery; ischemic - focal ischemia for 1 hour, without reperfusion; ischemic + intraischemic hypothermia; ischemic + previous intravenous ketoprofen, and ischemic + hypothermia and ketoprofen. Ten animals from each experimental group were used to establish the volume of infarct. Transient focal cerebral ischemia was obtained in rats by occlusion of the middle cerebral artery with an intraluminal suture. The infarct volume was measured using morphometric analysis of infarct areas defined by triphenyl tetrazolium chloride and the patterns of expression of the protein and gene NMDA were evaluated by immunohistochemistry and quantitative real-time PCR, respectively. Increases in the protein and gene NMDA receptor in the ischemics areas were observed and these increases were reduced by hypothermia and ketoprofen. The increase in the NMDA receptor protein and gene expression observed in the ischemic animals was reduced by neuroprotection (hypothermia and ketoprofen). The NMDA receptor increases in the ischemic area suggests that the NMDA mediated neuroexcitotoxicity plays an important role in cell death and that the neuroprotective effect of both, hypothermia and ketoprofen is directly involved with the NMDA...


NMDAR (N-metil-D-aspartato) es un tipo de receptor de glutamato ionotrópico y está ampliamente distribuido en el sistema nervioso central (SNC). En el SNC de mamíferos, NMDAR se destaca de manera importante en el proceso fisiopatológico de la isquemia cerebral. Este estudio tuvo como objetivo investigar el patrón de expresión de proteínas y genes para el NMDA neurotransmisor excitatorio experimental de la isquemia cerebral focal y el vacío en la neuroprotección con hipotermia y ketoprofeno. Se dividieron 120 ratas aleatoriamente en grupos de 6 animales cada uno (20): Control - sin cirugía; Sham - simulación de cirugía; isquémicas - isquemia focal durante 1 hora, sin reperfusión isquémica; hipotermia intra-isquémica; isquemia; previa aplicación de ketoprofeno intravenoso, e hipotermia isquémica y ketoprofeno. Diez animales de cada grupo experimental fueron utilizados para establecer el volumen de infarto.La isquemia cerebral focal transitoria fue obtenida en ratas mediante oclusión de la arteria cerebral media con una sutura intraluminal. El volumen de infarto fue medido mediante análisis morfométrico de las áreas de infarto definidas por cloruro de trifenil tetrazolio y patrones de expresión de la proteína y el gen de NMDA, fueron evaluados por inmunohistoquímica y PCR cuantitativa en tiempo real, respectivamente. Se observaron aumentos en la proteína y en el gen del receptor de NMDA en las áreas isquémicas y estos aumentos fueron reducidos por la hipotermia y ketoprofeno. El aumento de la proteína del receptor de NMDA y la expresión génica observada en los animales isquémicos fue reducido mediante hipotermia y ketoprofeno. Los aumentos del receptor de NMDA en el área isquémica sugiere que la neuro excitotoxicidad mediada por NMDA desempeña un papel importante en la muerte celular y que el efecto neuroprotector de ambos, hipotermia y ketoprofeno está directamente relacionado al NMDA...


Subject(s)
Animals , Rats , Brain Ischemia/metabolism , Brain Ischemia/pathology , Receptors, N-Methyl-D-Aspartate/metabolism , Ketoprofen/metabolism , Neuroprotective Agents/metabolism , Gene Expression , Hypothermia , Immunohistochemistry , Real-Time Polymerase Chain Reaction , Receptors, N-Methyl-D-Aspartate/genetics
14.
Indian J Biochem Biophys ; 2011 Apr; 48(2): 73-81
Article in English | IMSEAR | ID: sea-135303

ABSTRACT

Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily. PPAR-alpha is involved in wound healing, stimulation of lipid and folic acid catabolism, inflammation control, inhibition of ureagenesis and peroxisome proliferation. The PPAR/ is involved wound healing, cell proliferation, embryo implantation, adipocyte differentiation, myelination alteration and apoptosis. The PPAR is involved in fat, lipid and calorie utilization, sugar control, inflammation control and macrophage (MQ) matutation. Homocysteine (Hcy) binds to nuclear peroxisome proliferator activated receptor. Increase in PPAR expression decreases the level of nitrotyrosine and increases endothelial nitric oxide concentration, decreases metalloproteinase activity and expression as well as elastinolysis and reverses Hcy-mediated vascular dysfunction. The PPAR initially recognized as a regulator of adipocyte development has become a potential therapeutic target for the treatment of diverse disorders. In addition, the activation of PPAR receptor ameliorates neurodegenerative disease. This review focuses on the recent knowledge of PPAR in neuroprotection and deals with the mechanism of neuroprotection of central nervous system disorder by PPAR.


Subject(s)
Animals , Brain Ischemia/metabolism , Brain Ischemia/pathology , Brain Ischemia/therapy , Cell Death , Central Nervous System/cytology , Central Nervous System/metabolism , Central Nervous System/pathology , Cytoprotection , Humans , Neurodegenerative Diseases/metabolism , Neurodegenerative Diseases/pathology , Neurodegenerative Diseases/therapy , Neurons/cytology , Neurons/pathology , Neuroprotective Agents/metabolism , PPAR gamma/metabolism
15.
Article in English | IMSEAR | ID: sea-135346

ABSTRACT

Ischaemic stroke is a disorder involving multiple mechanisms of injury progression including activation of glutamate receptors, release of proinflammatory cytokines, nitric oxide (NO), free oxygen radicals and proteases. Presently, recombinant tissue plasminogen activator (rtPA) is the only drug approved for the management of acute ischaemic stroke. This drug, however, is associated with limitations like narrow therapeutic window and increased risk of intracranial haemorrhage. A large number of therapeutic agents have been tested including N-methly-D-aspartate (NMDA) receptor antagonist, calcium channel blockers and antioxidants for management of stroke, but none has provided significant neuroprotection in clinical trials. Therefore, searching for other potentially effective drugs for ischaemic stroke management becomes important. Immunosuppressive agents with their wide array of mechanisms have potential as neuroprotectants. Corticosteroids, immunophilin ligands, mycophenolate mofetil and minocycline have shown protective effect on neurons by their direct actions or attenuating toxic effects of mediators of inflammation. This review focuses on the current status of corticosteroids, cyclosporine A, FK506, rapamycin, mycophenolate mofetil and minocycline in the experimental models of cerebral ischaemia.


Subject(s)
Brain Ischemia/drug therapy , Brain Ischemia/pathology , Cell Death/physiology , Fibrinolytic Agents/therapeutic use , Humans , Immunosuppressive Agents/therapeutic use , Nerve Degeneration/pathology , Nerve Degeneration/physiopathology , Neuroprotective Agents/therapeutic use , Steroids/therapeutic use , Stroke/drug therapy , Stroke/pathology , Tissue Plasminogen Activator/therapeutic use
16.
Acta cir. bras ; 26(supl.1): 32-37, 2011. graf, tab
Article in English | LILACS | ID: lil-600654

ABSTRACT

PURPOSE: This study aimed to assess the effects of preconditioning with mixtures of oils containing high/low ratio of ω-6/ω-3 and ω-9/ω-6, respectively, in an experimental model of cerebral ischemia-reperfusion (I/R). METHODS: Forty-two Wistar rats were randomly distributed into two groups: control (n=24) and test (n=18). Control group was subdivided in 4 subgroups (n=6): G1: Sham-Water; G2: I/R-Water; G3: Sham-Isolipidic and G4: I/R-Isolipid. The animals received water or a isolipid mixture containing ω-3 oils (8:1 ratio) and ω-9/ω-6 (0.4:1 ratio) by gavage for seven days. Test group included 3 subgroups (n=6) G5: I/R-Mix1, G: 6 I/R-Mix2 and G7: I/R-Mix3. Test group animals received oily mixtures of ω-3 (1.4:1 ratio) and ω-6 (3.4:1 ratio), differing only in source of ω-3: G5 (alpha-linolenic acid); G6 (alpha-linolenic, docosahexaenoic and eicosapentaenoic acids), and G7 (alpha-linolenic and docosahexaenoic acids). On day 7 I/R rats underwent cerebral ischemia with bilateral occlusion of common carotid arteries for 1 hour followed by reperfusion for 3 hours. G1 and G3 animals underwent sham operation. Concluded the experiment, animals were decapitated and their brains sliced for red neurons (RN) count in CA3 area of the hippocampus. Variables were compared using ANOVA-Tukey test. RESULTS: The use of different mix preparations promoted a decrease in red cell count in all three groups (G5/G6/G7), compared with G2/G4, confirming the protective effect of different oil blends, regardless of ω-3 source. CONCLUSION: Pre-conditioning with mixtures of oils containing high ratio ω-6/ω-3 and low ω-9/ω-6 relationship protects brain neurons against I/R injury in an experimental model.


OBJETIVO: Avaliar os efeitos do pré-condicionamento com misturas de óleos contendo relação alta/baixa de ω-6/ω-3 e ω-9/ω-6, respectivamente, em um modelo experimental de isquemia/reperfusão (I/R) cerebral. MÉTODOS: Quarenta e dois ratos foram distribuídos aleatoriamente em dois grupos: controle (n=24) e teste (n=18). Grupo controle foi subdividido em quatro subgrupos (n=6): G1: Sham-Água; G2: I/R-Água; G3: Sham-Isolipídico e G4: I/R-Isolipídico. Os animais receberam água ou uma mistura isolipidica contendo ω-6/ω-3 óleos (8:1) e ω-9/ω-6 (0,4:1) por gavagem, durante sete dias. O grupo teste incluiu três subgrupos (n=6) G5: I/R-Mix1, G: 6 I/R-Mix2 e G7: I/R-Mix3. Animais do grupo teste receberam de misturas de óleos ω-6/ω-3 (1,4:1) e ω-9/ω-6 (3,4:1), diferindo apenas na fonte de -3: G5:alpha-linolênico; G6: ácidos alpha-linolênico, eicosapentaenóico e docosahexaenóico e G7:ácidos alpha-linolênico e docosahexaenóico. No 7º dia os grupos I/R foram submetidos à isquemia cerebral (1h) por oclusão bilateral das artérias carótidas comuns seguida de reperfusão (3h). Ratos G1 e G3 foram submetidos à operação simulada. Concluído o experimento, os animais foram decapitados e seus cérebros fatiados para contagem dos neurônios vermelhos na área CA3 do hipocampo. As variáveis foram comparadas pelo teste de ANOVA-Tukey. RESULTADOS: A utilização de diferentes misturas de óleos promoveu uma diminuição na contagem de células vermelhas nos grupos G5/G6/G7, em comparação com G2/G4, confirmando o efeito protetor das misturas de óleos, independentemente da origem de ω-3. CONCLUSÃO: O pré-condicionamento com misturas de óleos contendo alta proporção de ω-6/ω-3 e baixa proporção de ω-9/ω-6 protege os neurônios cerebrais da lesão de I/R em um modelo experimental.


Subject(s)
Animals , Male , Rats , Brain Ischemia/prevention & control , Fatty Acids/pharmacology , Ischemic Preconditioning/methods , Reperfusion Injury/prevention & control , Brain Ischemia/pathology , Cell Count , Disease Models, Animal , Drug Combinations , /pharmacology , /pharmacology , Neurons/chemistry , Random Allocation , Rats, Wistar , Time Factors
17.
Acta cir. bras ; 25(5): 428-433, Sept.-Oct. 2010. ilus, tab
Article in English | LILACS | ID: lil-558729

ABSTRACT

PURPOSE: To assess a rat model of cerebral ischemia induced by occlusion of the middle cerebral artery and its effect on the area of cerebral infarction. METHODS: Brain ischemia was induced in 52 male Wistar rats by introduction of a 3-0 nylon suture into the middle cerebral artery for either 90 (n=28) or 120 (n=24) minutes. Ischemic injury volume was determined by TTC staining, digital photography and analysis with the Image J software. Statistical analysis employed Student’s t test and the Mann-Whitney U test. RESULTS: The groups were similar in terms of weight (p=0.59). The length of thread inserted was 14.7 mm in the 90 min group and 20.2 mm in the 120 min group (p=0.37). Ischemic injury was detected in 11 animals (39 percent) after 90 min and 11 (45 percent) after 120 min (p=0.77). In animals exhibiting injury, filament length was 16.1±11 mm (90 min) vs. 21.9±7.4 mm (120 min) (p=0.15). The mean infarction zone volume was greater after 120 (259.2 mm³) than after 90 min (162.9 mm³) (p=0.04). The neurological deficit score for the 90 and 120 min groups was 2.0 and 2.4, respectively (p=0.84). CONCLUSION: The experimental model induced significant ischemic cerebral injury in both groups.


OBJETIVO: Avaliar o modelo de isquemia cerebral por oclusão da artéria cerebral média, mediante introdução de fio intraluminal por 90 e 120 minutos, e seu efeito sobre a área de infarto cerebral em ratos. MÉTODOS: 52 ratos machos Wistar foram submetidos à isquemia cerebral por introdução de fio de nylon 3-0 na artéria cerebral média por 90 ou 120 minutos. O volume da lesão isquêmica foi determinado pelo corante TTC, fotografia digital e utilização do programa ImageJ. Na análise estatística, foi utilizado o teste t- student e o U de Mann-Whitney. RESULTADOS: O comprimento do fio introduzido foi de 14,7 mm no grupo 90 minutos e 20,2 mm no grupo 120 minutos. Lesão isquêmica foi detectada em 11 animais (39 por cento) no grupo que de 90 minutos e 11 (45 por cento) do grupo de 120 minutos. Nos animais que apresentaram lesão, o comprimento do fio foi de 16,1±11 mm (90 minutos) e 21,9±7,4 mm (120 minutos). O volume médio da área de infarto foi maior no grupo 120 minutos do que no grupo 90 minutos. O escore de déficit neurológico foi de 2,0 no grupo 90 minutos e de 2,4 no grupo 120 minutos. CONCLUSÃO: O modelo experimental estudado induz lesão isquêmica cerebral significativa em ambos os grupos.


Subject(s)
Animals , Male , Rats , Brain Ischemia , Disease Models, Animal , Middle Cerebral Artery/surgery , Brain Ischemia/etiology , Brain Ischemia/pathology , Neurologic Examination , Rats, Wistar , Statistics, Nonparametric , Sutures , Time Factors
18.
Braz. j. med. biol. res ; 41(11): 1029-1036, Nov. 2008. ilus, tab, graf
Article in English | LILACS | ID: lil-500360

ABSTRACT

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99 percent, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97 percent, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.


Subject(s)
Animals , Male , Rats , Brain Ischemia/complications , Cerebral Cortex/pathology , Fever/complications , Nerve Degeneration/etiology , Brain Ischemia/pathology , Chronic Disease , Rats, Wistar , Time Factors
19.
Hamdard Medicus. 2008; 51 (3): 5-12
in English | IMEMR | ID: emr-102197

ABSTRACT

During past few years identification of many molecules that participate in neuronal death and particularly apoptosis by various experimental studies, has contributed to the information on pathogenesis of ischemic brain injury and oxidative stress has been regarded as one of the mechanisms. The present study has been undertaken to evaluate a free radical, as a measure of lipid peroxidation in patients with cerebral infarction and haemorrhage and also to correlate its level with lesion size and its outcome in the patient. The study included 50 patients of stroke [25 each with infarction and haemorrhage] while 25 comparable subjects served as control. Serum malondialdehyde [SMDA] levels was estimated on the first day of admission in both the study groups as a measure of lipid peroxidation status in these subjects and the lesion size was measured by computed tomography. The mean SMDA level in thrombotic and haemorrhagic group was 4.16 +/- 0.04 nmol/dL and 4.03 +/- 1.1 nmol/dL while it was 1.9 +/- 0.4 nmol/dL in control. The difference in the mean SMDA levels in the controls and study subjects were statistically significant [p<0.001], while the difference between the thrombotic and haemorrhagic groups was statistically insignificant. The mean size of large lesion in thrombotic group was 13.6 +/- 3.0 cm[2] while it was 5.0 +/- 1.4 cm[2] for small lesions. The corresponding values of SMDA with these lesions were 4.98 +/- 0.9 nmol/dL and 3.23 +/- 0.4 nmol/dL. In haemorrhagic group mean size of large lesion was 13.3 +/- 1.9 cm[2] while that of small lesion was 6.6 +/- 1.9 cm[2]. The respective SMDA levels were 5.0 +/- 0.7 nmol/dL and 3.13 +/- 0.2 nmol/dL. There was marked statistical significance [p<0.001] in the SMDA levels between the small and large lesions in both study groups. A significant correlation existed between serum MDA levels, lesion size and early outcome in patients with stroke [p<0.001]. It is, therefore, concluded that the SMDA levels are raised in patients with acute stroke and hence are an indicator of the involvement of lipid peroxidation in its pathophysiology and can also be used as a prognostic markers in subjects with stroke


Subject(s)
Humans , Malondialdehyde/blood , Brain Ischemia/pathology , Stroke/physiopathology , Oxidative Stress , Lipid Peroxides/blood , Biomarkers
20.
Arq. bras. cardiol ; 88(2): e32-e35, fev. 2007. ilus
Article in Portuguese | LILACS | ID: lil-444370

ABSTRACT

Relatamos o caso de uma criança de 11 anos, com doença renal crônica e hiperparatireoidismo secundário. Havia sido tratada com diálise, calcitriol, carbonato de cálcio e, na evolução, apresentou dislipidemia e trombos calcificados em vários vasos e órgãos. O exame anatomopatológico revelou necrose cerebral isquêmica, calcificação nas artérias coronárias e infarto do miocárdio.


We describe a case 11 year-old boy, in which a chronic renal disease and secondary hyperparathyroidism was treated by dyalisis, calcitriol, and calcium supplementation. He developed dyslipidemia, calcified lesions with thrombus formation in several organs and vessels. Necropsy findings showed ischemic cerebral necrosis, calcification in arteries including coronaries, and myocardial infarction.


Subject(s)
Humans , Male , Child , Brain Ischemia/etiology , Kidney Failure, Chronic/complications , Myocardial Infarction/etiology , Brain Ischemia/pathology , Calcinosis , Fatal Outcome , Kidney Failure, Chronic/pathology , Myocardial Infarction/pathology , Severity of Illness Index
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