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Resumen: El síndrome de QT largo adquirido puede ser secundario a la hipotermia, tanto accidental como terapéutica. Es poco el conocimiento sobre el efecto de ésta en la actividad eléctrica cardíaca, sobre todo en recién nacidos, y sus potenciales complicaciones. Se presenta el caso clínico de un recién nacido con diagnóstico de encefalopatía hipóxico isquémica que presenta una prolongación del intervalo QT durante el tratamiento con hipotermia. Se discute la evolución del paciente, que es consistente con lo referido en la literatura sobre el tema: buena evolución, ausencia de arritmias graves o alteraciones hemodinámicas, y normalización del electrocardiograma luego de finalizado el tratamiento.
Summary: Acquired long QT syndrome may be secondary to hypothermia, both accidental and therapeutic. There is not enough knowledge about the effect of hypothermia in cardiac activity and its potential complications, especially in newborns. We present the clinical case of a newborn with a diagnosis of hypoxic ischemic encephalopathy who has a prolonged QT interval during treatment with hypothermia. The evolution of the patient is discussed, which is consistent with what is referred to in the literature on the subject: Good evolution, absence of serious arrhythmias or hemodynamic alterations, and normalization of the ECG after the end of treatment.
Resumo: A síndrome do QT longo adquirida pode ser secundária à hipotermia, tanto acidental quanto terapêutica. Pouco se sabe sobre seu efeito na atividade elétrica cardíaca, principalmente em recém-nascidos, e suas possíveis complicações. Apresentamos o relato de caso clínico de um recém-nascido com diagnóstico de encefalopatia hipóxica isquêmica que apresenta prolongamento do intervalo QT durante o tratamento com hipotermia. Discutimos a evolução do paciente, a que é consistente com a literatura sobre o assunto: boa evolução, ausência de arritmias graves ou alterações hemodinâmicas e normalização do ECG após o término do tratamento.
ABSTRACT
OBJECTIVE: Hypoxic-ischemic (HI) brain injury in the human perinatal period often leads to significant long-term neurobehavioral dysfunction in the cognitive and sensory-motor domains. Using a neonatal HI injury model (unilateral carotid ligation followed by hypoxia) in postnatal day seven rats, the present study investigated the long-term effects of HI and potential behavioral protective effect of pentoxifylline. METHODS: Seven-day-old rats underwent right carotid ligation, followed by hypoxia (FiO2 = 0.08). Rats received pentoxifylline immediately after and again 2 hours after hypoxia (two doses, 60–100 mg/kg/dose), or serum physiologic. Another set of seven-day-old rats was included to sham group exposed to surgical stress but not ligated. These rats were tested for spatial learning and memory on the simple place task in the Morris water maze from postnatal days 77 to 85. RESULTS: HI rats displayed significant tissue loss in the right hippocampus, as well as severe spatial memory deficits. Low-dose treatment with pentoxifylline resulted in significant protection against both HI-induced hippocampus tissue losses and spatial memory impairments. Beneficial effects are, however, negated if pentoxifylline is administered at high dose. CONCLUSION: These findings indicate that unilateral HI brain injury in a neonatal rodent model is associated with cognitive deficits, and that low dose pentoxifylline treatment is protective against spatial memory impairment.
Subject(s)
Animals , Humans , Rats , Hypoxia , Brain Injuries , Brain , Cognition Disorders , Hippocampus , Hypoxia-Ischemia, Brain , Learning , Ligation , Memory , Pentoxifylline , Rodentia , Spatial Learning , Spatial Memory , WaterABSTRACT
We report an extremely rare case of a patient with hypoxic-ischemic brain injury who recovered consciousness and motor and cognitive functions due to paradoxical response after zolpidem administration. A 32-year-old woman who had attempted suicide by hanging was admitted. The patient had stabilized in a state of drowsy mentality, quadriparesis, dysphagia, and impaired cognition. Brain magnetic resonance imaging was suggestive of hypoxic ischemic brain injury and unilateral infarction in the right posterior cerebral artery territory. Due to sleep disturbance, zolpidem was administered, and paradoxically consciousness level and function returned to near-normal during the duration of the drug-effect. In addition to previous reports, our case characteristically showed remarkable motor and cognitive function recovery, not only consciousness level. The drug-effect time was gradually decreased after 18 months and absent after 3 years. We have reviewed related literature and discussed possible neuropharmacological and neurobiological mechanism.
Subject(s)
Adult , Female , Humans , Brain Injuries , Brain , Cognition , Consciousness , Deglutition Disorders , Hypoxia-Ischemia, Brain , Infarction , Infarction, Posterior Cerebral Artery , Magnetic Resonance Imaging , Posterior Cerebral Artery , Quadriplegia , Suicide, AttemptedABSTRACT
PURPOSE: Hypoxic-ischemic encephalopathy is a significant cause of neonatal morbidity and mortality. Erythropoietin (EPO) is emerging as a therapeutic candidate for neuroprotection. Therefore, this study was designed to determine the neuroprotective role of recombinant human EPO (rHuEPO) and the possible mechanisms by which mitogen-activated protein kinase (MAPK) signaling pathway including extracellular signal-regulated kinase (ERK1/2), JNK, and p38 MAPK is modulated in cultured cortical neuronal cells and astrocytes. METHODS: Primary neuronal cells and astrocytes were prepared from cortices of ICR mouse embryos and divided into the normoxic, hypoxia (H), and hypoxia-pretreated with EPO (H+EPO) groups. The phosphorylation of MAPK pathway was quantified using western blot, and the apoptosis was assessed by caspase-3 measurement and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. RESULTS: All MAPK pathway signals were activated by hypoxia in the neuronal cells and astrocytes (P<0.05). In the neuronal cells, phosphorylation of ERK-1/-2 and apoptosis were significantly decreased in the H+EPO group at 15 hours after hypoxia (P<0.05). In the astrocytes, phosphorylation of ERK-1/-2, p38 MAPK, and apoptosis was reduced in the H+EPO group at 15 hours after hypoxia (P<0.05). CONCLUSION: Pretreatment with rHuEPO exerts neuroprotective effects against hypoxic injury reducing apoptosis by caspase-dependent mechanisms. Pathologic, persistent ERK activation after hypoxic injury may be attenuateed by pretreatment with EPO supporting that EPO may regulate apoptosis by affecting ERK pathways.
Subject(s)
Animals , Humans , Mice , Hypoxia , Apoptosis , Astrocytes , Blotting, Western , Caspase 3 , DNA Nucleotidylexotransferase , Embryonic Structures , Erythropoietin , Hypoxia-Ischemia, Brain , MAP Kinase Signaling System , Mice, Inbred ICR , Mitogen-Activated Protein Kinases , Mortality , Neurons , Neuroprotection , Neuroprotective Agents , p38 Mitogen-Activated Protein Kinases , Phosphorylation , Phosphotransferases , Protein KinasesABSTRACT
Resumen Objetivo: caracterizar la población con diagnóstico de epilepsia en el Hospital Infantil Universitario Rafael Henao Toro, en Manizales (Colombia), desde el punto de vista del comportamiento de la enfermedad, factores de riesgo, tratamiento y particularidades demográficas. Métodos: estudio de corte transversal realizado mediante la revisión de historias clínicas.Resultados: de 172 pacientes, 51,2 % fueron del género masculino; las crisis focales fueron las más frecuentes con 59,1 %; la comorbilidad más usual fue el retraso del desarrollo psicomotor (30,9 %), aunque si se tiene en cuenta la asociación con otras enfermedades la cifra asciende al 57,9 %; la monoterapia más utilizada fue el ácido valpróico (39,8 %). La epilepsia infantil se asoció con estados hipertensivos maternos en un 8,7 %; el 21,7 % presentó encefalopatía hipóxica-isquémica; 24,1 % tenían antecedentes familiares de epilepsia; en 15,1 % de los casos hubo bajo peso y 16,7 % de talla baja al nacer. Conclusión: los hallazgos de la presente investigación, en general, coinciden con lo reportado en otros estudios efectuados en poblaciones análogas.
Abstract Objective:To characterize the diagnosed with epilepsy population at the "Hospital Infantil Universitario Rafael Henao Toro", in the city of Manizales (Colombia) from the behavior of the disease, risk factors, treatment and demographic characteristics. Methods: Cross-sectional study of the population referred to and performed by reviewing medical records. Results: of 172 patients, 51,2% were male gender; focal seizures were the most frequent with 59.1%; the most common comorbidity was delayed psychomotor development (30.9%), although if is consider the association with other diseases the figure is 57.9%; the most commonly monotherapy used was Valproic Acid (39.8%). Childhood epilepsy was associated with maternal hypertensive disorders in 8,7%; 21.7% had hypoxic-ischemic encephalopathy; 24.1% had a family history of epilepsy; in 15.1 % of cases was underweight and 16.7% of short stature at birth. Conclusion: The findings of this research, in general, agree with those reported in other studies in similar populations.
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A escala mundial, la isquemia cerebral constituye una de las principales causas de muerte, por lo que los modelos animales de isquemia cerebral son extensamente usados tanto en el estudio de la pato-fisiología del fenómeno isquémico; como en la evaluación de agentes terapéuticos con posible efecto protector o regenerador. Los objetivos de este estudio fueron examinar la presencia de daño neuronal en diferentes áreas cerebrales como consecuencia del evento isquémico; así como evaluar consecuencias de este proceder sobre los procesos de memoria-aprendizaje. Los grupos de estudios incluyeron un grupo experimental de animales isquémicos, 30 ratas a las que se les ocluyó ambas arterias carótidas comunes, y un grupo control. Fue evaluada la expresión de genes isquémicos e inflamatorios por técnicas de qPCR 24 horas post lesión, la morfología del tejido cerebral en áreas de corteza, estriado e hipocampo, siete días post lesión y los procesos de memoria y aprendizaje, 12 días post lesión. Los estudios morfológicos evidenciaron que el proceder induce la muerte de poblaciones celulares en corteza, estriado e hipocampo; la isquemia modificó la expresión los genes gfap, ho-1, il-6, il-17 e ifn-γ, lo cual puede ser utilizado como un marcador de proceso isquémico temprano. Adicionalmente, el daño isquémico causó un deterioro en la memoria espacial. Esta caracterización nos permite contar con un modelo experimental donde desarrollar futuros estudios sobre la patofisiología de los eventos isquémicos y la evaluación de estrategias terapéuticas.
Cerebral ischemia is a major cause of death, for this reason animal models of cerebral ischemia are widely used to study both the pathophysiology of ischemic phenomenon and the evaluation of possible therapeutic agents with protective or regenerative properties. The objectives of this study were to examine the presence of neuronal damage in different brain areas following the ischemic event, and assess consequences of such activities on the processes of memory and learning. The study group included an experimental group ischemic animals (30 rats with permanent bilateral occlusion of the carotids), and a control group. Was evaluated gene expression and inflammatory ischemic by qPCR techniques 24h post injury, brain tissue morphology in areas of cortex, striatum and hippocampus seven days post injury and processes of memory and learning, 12 days post injury. The morphological studies showed that the procedure induces death of cell populations in cortex, striatum and hippocampus, ischemia modified gfap gene expression and ho, il-6, il-17 and ifn-γ, which can be used as a marker of early ischemic process. Additionally, the ischemic injury caused spatial memory decline. This characterization gives us an experimental model to develop future studies on the pathophysiology of ischemic events and assessing therapeutic strategies.
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Objective To study the effect of local mild hypothermia on AKT protein expression after rats focal cerebral ischemia-reperfusion injury.Methods By using the model of rat focal cerebral ischemia-reperfusion injury,the middle cerebral arteries(MCA)of SD rats were occluded for 2 h,and reperfused for2h,12h,24h,72h.Immunohistochemical analysis was used to detect expression of AKT.Results AKT expressed after ischemia 2h,the expression was significantly increased after ischemia reperfusion with peak expression at 72h in model group on normal temperature.In mild hypothermia group,the AKT expression was higher than that in normal temperature group when at the same time point.Conclusion Brain hypoxia-ischemia could induce the expression of AKT.Mild hypothermia could promote the expression of AKT.The expression of AKT could be one of the protected way of brain hypoxia-ischemia.
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Objective To explore the role of tissue-type plasminogen activator(tPA) in neonatal rat with hypoxia-ischemia brain damage(HIBD).Methods Seven-day-old Wistar rat pups were used for the Vannucci model of HIBD.Reverse transcription-polymerase chain reaction(RT-PCR),terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL),double immunostaining and immunoblot analysis were adapted to determin the expression of tPA at acute phase after HIBD and neural cell apoptosis and the blood-brain-barrier(BBB) damage.Results Neonatal hypoxia-ischemia triggers persistent induction of the plasminogen system.The increase of tPA activity induced the degradation of laminin and occludin which would aggravate the BBB damage.The number of neural cell apoptosis after HIBD increased progressively with the reperfusion time.Conclusions The increase of tPA at the acute phase after HIBD can help clot to dissolve,while its extravascular proteolysis will induce cell apoptosis and BBB damage which will aggravate brain injury.
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Objective To explore the effects of brain derived neurotrophic factors (BDNF) on concentrations of cerebral endogenous opioid peptides(EOP)in neonatal rats subject to with hypoxic ischemic brain injury (HIBI). Methods Seven day old Sprague Dawley rats were randomly divided into a HIBI+BDNF group (group A),a HIBI group (group B) and a sham operation group (group C). Models of HIBI were established by use of permanent ligation of the left common carotid artery followed by 2.5 hours ofinhalation of 8%O 2+92%N 2, then 0.5 ?g BDNF was injected into the parietal cerebral ventricle in group A immediately. Contents of dynorphin A 1 13 like, ? endorphin like and leu enkaphalin like immunoreactivities (ir DynA 1 13 , ir ? EP and ir LEK) in cortex and hippocampus were measured at 0, 60, 120 min after administration of BDNF. Results The concentrations of ir DynA 1 13 and ir ? EP in the cortex and hippocampus in group B were increased significantly than those in group C at most time points( P
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Objective To understand the mechanism of cerebral energy failure after hypoxia ischemia at the molecular level and to establish the protocol for the safe and effective treatment of hypoxic-ischemic encephalopathy(HIE).Methods One hundred neonatal rats were divided into normal control group and hypoxic-ischemic(HI) group. SD rats of both groups were decapitated at the time of 2 h,24 h,48 h,72 h and 7 d after HI.These tissues of cerebrum,cortex and hippocampus were taken out to explore the influence of HI on the expression of GLUT1 and GLUT3 genes with the method of RT-PCR.Results There was an enhancement in the expression of GLUT1 and GLUT3 genes with the increasing of day age. The expression was more intense in hippocampus than that in cortex. However, HI could significantly enhance the expression of GLUT genes. The expression was higher in cortex than that in hippocampus. The expression of two genes reached the peak at 24 h after HI, but was significantly lower than that in control group at 7 d after HI.Conclusion The increased expression of GLUT genes can maintain the energy supplement for the brain and delay a cascade reaction of cerebral energy failure.