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1.
J Dig Dis ; 13(5): 267-73, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22500789

RESUMO

OBJECTIVE: The aim of this study was to summarize the clinical features of autoimmune pancreatitis (AIP) and review the advances in the differential diagnosis with pancreatic carcinoma, thus help to make a correct diagnosis and avoid unnecessary surgery in clinical practice. METHODS: Five patients diagnosed as AIP in accordance with the HISORt criteria in Zhongshan Hospital, Fudan University from 2008 to 2010 were enrolled in the study. Clinical features were analyzed and related literature was reviewed. RESULTS: Progressive jaundice and abdominal pain were the most frequent symptoms, as well as weight loss, together with serological changes such as elevation of alkaline phosphatase, γ-glutamyl-transpeptidase and serum bilirubin. Two of them showed high serum immunoglobulin G4 (IgG4) levels. Both focal and diffuse changes were found on computed tomography and magnetic resonance imaging. Two of our patients underwent operation because of a high suspicion of malignant tumor, and steroid therapy was administered to the other three patients diagnosed as AIP. No relapse was observed during the follow-up duration of all the patients. CONCLUSIONS: Although some recent advances have been made to help the diagnosis of AIP, the differentiation between AIP and pancreatic carcinoma is still a challenge. Clinicians must remember to exclude AIP before making a diagnosis of pancreatic carcinoma.


Assuntos
Doenças Autoimunes/diagnóstico , Imunoglobulina G/sangue , Neoplasias Pancreáticas/diagnóstico , Pancreatite/diagnóstico , Adulto , Idoso , Biomarcadores/sangue , Diagnóstico Diferencial , Humanos , Icterícia/etiologia , Masculino , Pessoa de Meia-Idade , Pancreatite/imunologia
2.
Am J Chin Med ; 38(2): 307-18, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20387227

RESUMO

Previous studies have shown that the bisbenzyl isoquinoline alkaloid dauricine can protect the brain against ischemic damage. We investigated here whether dauricine could inhibit neuronal apoptosis and modulate Bcl-2 family protein levels in a rat model of transient focal cerebral ischemia. Male Sprague-Dawley rats underwent a 60 min temporary occlusion of the middle cerebral artery (MCAO). Two doses of dauricine (5 and 10 mg/kg as low and high dose respectively) were administered intraperitoneally at 1 hour after MCAO. After neurological deficits were assessed at 3 hours and 24 hours of reperfusion, rats were killed and brain samples were collected. Apoptotic changes were evaluated by TUNEL method. The immunohistochemistry and Western blot were used to assess the protein expressions of Bcl-2 and Bax. RT-PCR was used to determine Bcl-2 and Bax mRNA expressions. Dauricine (5 and 10 mg/kg) treatment improved neurological deficits, diminished DNA fragmentation, increased Bcl-2 expression and reduced Bax expression in the penumbra. The infarct-reducing effects of dauricine may be due, in part, to the inhibition of apoptotic cell death via modulation Bcl-2 family protein in the penumbra.


Assuntos
Benzilisoquinolinas/farmacologia , Infarto da Artéria Cerebral Média/patologia , Fármacos Neuroprotetores/farmacologia , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Tetra-Hidroisoquinolinas/farmacologia , Animais , Apoptose , Western Blotting , Modelos Animais de Doenças , Imuno-Histoquímica , Infarto da Artéria Cerebral Média/metabolismo , Masculino , Proteínas Proto-Oncogênicas c-bcl-2/genética , RNA Mensageiro/genética , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase Via Transcriptase Reversa
3.
Am J Chin Med ; 38(1): 37-49, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20128043

RESUMO

Our previous studies have shown that daurisoline (DS) exerted antiarrhythmic effects on various experimental arrhythmias. In this study, the effects of DS on early afterdepolarizations (EADs) and its possible mechanisms have been investigated. Cardiac hypertrophy was induced in rabbits by coarctating the abdominal aorta. The effects of DS on action potential duration (APD) and the incidences of EADs were studied in hypertrophied papillary muscles of rabbits in the conditions of low external K(+) concentration ([K(+)]o) and dofetilide (dof) by using standard microelectrode technique. The whole-cell patch clamp was used to record the L-type calcium current (I(Ca-L)) in isolated left ventricular cells of rabbits. The results showed that in hypertrophied papillary muscles of rabbits with low [K(+)]o ([K(+)]o = 2.7 mM), 1 microM dof prolonged APD(50) and APD(90) markedly and the incidence of EADs was 66.7% (4/6, p < 0.01); when 15 microM DS was applied, the incidence of EADs was 0% (0/4, p < 0.01) and the prolonged APD was shortened (p < 0.01). In a single myocyte, DS could also inhibit EADs induced by dof, low [K(+)]o and low external Mg(2+) concentration ([Mg(2+)]o) ([Mg(2+)](o) = 0.5 mM). DS could decrease the triangulation. In a single myocyte, DS could make the I-V curve upward, shift the steady-state activation curves to the right and the steady-state inactivation curves to the left and prolong the tau value of recovery curve obviously. These results suggested that DS could inhibit EADs which may be associated with its blockade effects on I(Ca-L).


Assuntos
Potenciais de Ação/efeitos dos fármacos , Antiarrítmicos/farmacologia , Benzilisoquinolinas/farmacologia , Canais de Cálcio Tipo L/efeitos dos fármacos , Coração/efeitos dos fármacos , Menispermum/química , Extratos Vegetais/farmacologia , Animais , Antiarrítmicos/isolamento & purificação , Antiarrítmicos/uso terapêutico , Benzilisoquinolinas/isolamento & purificação , Benzilisoquinolinas/uso terapêutico , Sinalização do Cálcio/efeitos dos fármacos , Cardiomegalia/tratamento farmacológico , Modelos Animais de Doenças , Coração/fisiologia , Células Musculares/efeitos dos fármacos , Técnicas de Patch-Clamp , Fenetilaminas , Fitoterapia , Extratos Vegetais/química , Extratos Vegetais/uso terapêutico , Potássio/metabolismo , Coelhos , Rizoma , Sulfonamidas , Fatores de Tempo
4.
Can J Physiol Pharmacol ; 87(11): 954-62, 2009 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-19935903

RESUMO

We have previously reported that dauricine exerted antiarrhythmic effects on various experimental arrhythmias. To further clarify its mechanism, the effects of dauricine on action potential duration (APD), early afterdepolarizations (EADs), triangulation, which is defined as the repolarization time from APD at 30% level (APD30) to APD at 90% level (APD90), and L-type calcium current (I(Ca-L)) were studied using standard microelectrode techniques on rabbit papillary muscles and whole-cell patch clamp techniques on single myocytes isolated from rabbits by enzymatic digestion, respectively. Cardiac hypertrophy was induced by coarctating the abdominal aorta of rabbits. The results showed that in papillary muscles of hypertrophied rabbits, 1 micromol/L dofetilide, a selective IKr blocker, prolonged APD50 and APD90 and induced EADs (4/6, p < 0.01) with hypokalemia ([K+]o = 2.7 mmol/L). Dauricine inhibited EADs (p < 0.01) and shortened the prolonged APD (p < 0.01). In single myocytes, dauricine also inhibited EADs induced by dofetilide, hypokalemia, and hypomagnesaemia. Dauricine decreased the triangulation and reduced the peak amplitude of I(Ca-L) at all potentials tested. Dauricine shifted the steady-state activation curves to the right and steady-state inactivation curves to the left and prolonged the tau value of the recovery curve. These results suggest that dauricine inhibits EADs and this effect may be associated with its blockade of I(Ca-L).


Assuntos
Antiarrítmicos/farmacologia , Benzilisoquinolinas/farmacologia , Bloqueadores dos Canais de Cálcio/farmacologia , Canais de Cálcio Tipo L/metabolismo , Hipertrofia Ventricular Esquerda/fisiopatologia , Fármacos Neuromusculares Despolarizantes/farmacologia , Músculos Papilares/efeitos dos fármacos , Tetra-Hidroisoquinolinas/farmacologia , Potenciais de Ação/efeitos dos fármacos , Animais , Relação Dose-Resposta a Droga , Feminino , Técnicas In Vitro , Síndrome do QT Longo/induzido quimicamente , Magnésio/metabolismo , Masculino , Miócitos Cardíacos/efeitos dos fármacos , Técnicas de Patch-Clamp , Fenetilaminas/farmacologia , Potássio/metabolismo , Bloqueadores dos Canais de Potássio/farmacologia , Coelhos , Sulfonamidas/farmacologia
5.
Antimicrob Agents Chemother ; 53(12): 5055-9, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19752279

RESUMO

Anti-Hantaan virus monoclonal antibody (AHM) is a murine monoclonal antibody against Hantaan virus being developed for the treatment of hemorrhagic fever with renal syndrome. The purpose of the present study was to describe the tolerance and pharmacokinetics of an intravenously administered single ascending dose of AHM in Chinese healthy volunteers. Four cohorts of 22 healthy subjects received AHM at 2.5 to 20 mg, and the results indicated that AHM was well tolerated. We established a highly sensitive, rapid, and accurate immunoassay for the kinetic analysis of AHM in serum. Serial blood samples were obtained after intravenous administration for up to 17 days. A one-compartment model was determined to best describe the disposition of AHM. The maximal level in serum and the area under the serum concentration-time curve were proportional to the doses. The mean clearance, the half-life, and the volume of distribution were constant, irrespective of the dose. AHM was slowly cleared and had a half-life of approximately 110 h. These data support the use of a treatment regimen in which AHM is given only once intravenously.


Assuntos
Anticorpos Monoclonais/farmacocinética , Antivirais/farmacocinética , Vírus Hantaan/imunologia , Animais , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais/efeitos adversos , Anticorpos Monoclonais/imunologia , Antivirais/administração & dosagem , Antivirais/efeitos adversos , Antivirais/imunologia , Área Sob a Curva , Ensaio de Imunoadsorção Enzimática , Feminino , Meia-Vida , Humanos , Injeções Intravenosas , Masculino , Camundongos , Adulto Jovem
6.
Can J Physiol Pharmacol ; 85(6): 621-7, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17823624

RESUMO

We have previously reported that dauricine protects brain tissues from focal cerebral ischemia. To corroborate this effect, neurotoxicity due to hypoxia and hypoglycemia was assessed in primary cultures of rat cortical neurons by using a trypan blue exclusion method. To further clarify the mechanism, the intracellular Ca2+ concentration ([Ca2+]i) and mitochondrial membrane potential (Deltapsim) of dissociated rat cortical cells were monitored by fura-2 fluorescence measurements and flow cytometry, respectively. The results showed that 1 and 10 micromol/L dauricine significantly enhanced neuronal survival during 4 h of hypoxia and hypoglycemia. Dauricine inhibited the increase in [Ca2+]i and decrease in Deltapsim induced by 30 min of hypoxia and hypoglycemia. When exploring the pathway, we found that 1 micromol/L dauricine inhibited the [Ca2+]i increase induced by 7.5 nmol/L thapsigargin in either the presence or absence of extracellular Ca2+ and by 1 mmol/L L-glutamate in the presence of extracellular Ca2+. These results suggest that dauricine prevents neuronal loss from ischemia in vitro, which is in accordance with our previous research in vivo. In addition, by inhibiting Ca2+ release from the endoplasmic reticulum and Ca2+ influx from the extracellular space, dauricine suppressed the increase in [Ca2+]i and, subsequently, the decrease in Deltapsim induced by hypoxia and hypoglycemia. This effect may underlie the mechanism of action of dauricine on cerebral ischemia.


Assuntos
Alcaloides/farmacologia , Benzilisoquinolinas/farmacologia , Cálcio/metabolismo , Neurônios/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Tetra-Hidroisoquinolinas/farmacologia , Animais , Animais Recém-Nascidos , Bloqueadores dos Canais de Cálcio/farmacologia , Hipóxia Celular , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Córtex Cerebral/citologia , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Retículo Endoplasmático/química , Retículo Endoplasmático/efeitos dos fármacos , Retículo Endoplasmático/metabolismo , Espaço Extracelular/química , Espaço Extracelular/efeitos dos fármacos , Espaço Extracelular/metabolismo , Homeostase/efeitos dos fármacos , Hipoglicemia/fisiopatologia , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Neurônios/citologia , Neurônios/metabolismo , Nimodipina/farmacologia , Ratos , Ratos Wistar
7.
Am J Chin Med ; 35(3): 477-86, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17597506

RESUMO

Our previous experimental studies showed that dauricine could protect the brain from ischemic damage, but the underlying mechanisms were unknown. In this study, we investigated the effect of dauricine on the changes of the inflammation process induced by ischemia/reperfusion (I/R). After I/R, the enzyme activity of MPO, the expression of ICAM-1 and the transcription of IL-1beta and TNF-alpha mRNA were all significantly increased (p < 0.01). And after treatment with dauricine, they were all significantly reduced compared to the vehicle-treated I/R group (p < 0.05 or p < 0.01). These results suggest that dauricin attenuates the inflammation process induced by I/R. The neuroprotective effect of dauricine may partly due to the inhibition acute inflammation induced by I/R.


Assuntos
Alcaloides/farmacologia , Anti-Inflamatórios não Esteroides/farmacologia , Benzilisoquinolinas/farmacologia , Encéfalo/metabolismo , Inflamação/prevenção & controle , Traumatismo por Reperfusão/tratamento farmacológico , Tetra-Hidroisoquinolinas/farmacologia , Animais , Encéfalo/irrigação sanguínea , Movimento Celular/efeitos dos fármacos , Inflamação/metabolismo , Molécula 1 de Adesão Intercelular/metabolismo , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Masculino , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Peroxidase/metabolismo , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/metabolismo , Transcrição Gênica , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
8.
Clin Exp Pharmacol Physiol ; 34(3): 177-84, 2007 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17250636

RESUMO

1. Previous experimental studies have shown that dauricine can protect the brain against ischaemic damage, but the underlying mechanisms remain unknown. In the present study, we examined whether dauricine inhibits neuronal apoptosis in the penumbra in a rat model of transient focal cerebral ischaemia. 2. Male Wistar rats underwent a 90 min temporary occlusion of the middle cerebral artery. Dauricine (21, 42 and 84 mg/kg) was administered by intragastric gavage twice a day for 3 days before ischaemia. Rats were killed and brain samples were collected 24 h after ischaemia. Histopathological outcome was evaluated by haematoxylin-eosin staining. Apoptotic changes were evaluated by terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling (TUNEL) for DNA fragmentation. The mitochondrial pathway was explored using immunohistochemistry for cytochrome c release, caspase 9 and caspase 3 activation, as well as by reverse transcription-polymerase chain reaction for determination of caspase 9 and caspase 3 mRNA expression. 3. Cytochrome c release, activation of caspase 9 and caspase 3 and DNA fragmentation were detected 24 h after ischaemia. Dauricine (42 and 84 mg/kg) pretreatment improved histopathological recovery, diminished DNA fragmentation and reduced cytochrome c release and activation of caspase 9 and caspase 3 in the penumbra at 24 h. 4. These findings suggest that dauricine attenuates apoptosis in the penumbra after transient focal cerebral ischaemia. The infarct-reducing effects of dauricine may be due, in part, to the inhibition of apoptotic cell death via a mitochondrial pathway in the penumbra.


Assuntos
Alcaloides/farmacologia , Apoptose/efeitos dos fármacos , Benzilisoquinolinas/farmacologia , Ataque Isquêmico Transitório/patologia , Mitocôndrias/metabolismo , Fármacos Neuroprotetores , Tetra-Hidroisoquinolinas/farmacologia , Animais , Caspase 3/metabolismo , Caspase 9/metabolismo , Citocromos c/metabolismo , Fragmentação do DNA/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Masculino , Mitocôndrias/efeitos dos fármacos , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa
9.
Am J Chin Med ; 33(6): 923-34, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16355449

RESUMO

Gap junction communication between astrocytes plays an important role in the brain. The purpose of this study was to investigate the effects of Gingko biloba extract (GBE) on the changes of connexin 43 (Cx43) mRNA and protein expression levels of rat cortex and hippocampus induced by ischemia-reperfusion and astrocyte gap junction intercellular communication (GJIC) induced by hypoxia-reoxygenation. After 2 hours of middle cerebral artery occlusion (MCAO) followed by 24 hours of reperfusion, there was obvious neurological deficit in rats. Cx43 mRNA and protein expression levels of rat cortex and hippocampus in the ischemia hemisphere were decreased significantly. When GBE at doses of 50 and 100 mg/kg body weight was administrated by p.o. daily for 7 days, the neurological deficit was improved, and lower Cx43 mRNA and protein expression levels induced by ischemia-reperfusion were recovered to normal. The i.p. injection of nimodipine (0.7 mg/kg weight body) also showed improvement on neurological deficit and Cx43 expression levels. Astrocyte GJIC was measured by the fluorescence recovery after photobleaching (FRAP). Hypoxia-reoxygenation induced a significant decrease in GJIC. Pretreatment with GBE (100 mg/l) and nimodipine (1.6 mg/l) significantly prevented the hypoxia-reoxygenation inhibition of GJIC. These results suggest that GBE could exert its neuroprotective effects by improvement of Cx43 expression and GJIC induced by hypoxia/ischemia-reoxygenation/ reperfusion injury.


Assuntos
Isquemia Encefálica/tratamento farmacológico , Junções Comunicantes/efeitos dos fármacos , Ginkgo biloba , Extratos Vegetais/farmacologia , Traumatismo por Reperfusão/tratamento farmacológico , Animais , Astrócitos/efeitos dos fármacos , Comunicação Celular/efeitos dos fármacos , Células Cultivadas , Conexina 43/metabolismo , Injeções Intraperitoneais , Masculino , Nimodipina/farmacologia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Vasodilatadores/farmacologia
10.
Yao Xue Xue Bao ; 40(3): 213-9, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15952591

RESUMO

AIM: To investigate glutamate-induced [Ca2+]i changes in cultured rat neonatal cortical astrocytes after hypoxia/reoxygenation, H2O2 or high concentration of L-glutamate injury. In the meantime, the effects of Gingko biloba extract (GbE) were examined. METHODS: [Ca2+]i changes in astrocytes were monitored by laser scanning confocal microscopy with the Ca2+ sensitive fluorescent probe fluo-3. RESULTS: After astrocytes were impaired by hypoxia/reoxygenation, H2O2 (50 micromol x L(-1)) or L-glutamate (0.25 mmol x L(-)), the exogenous glutamate (27 micromol x L(-1)) could not induce increase of [Ca2+]i, but decrease by (3.3 +/- 1.6)%, (81 +/- 11)% and (81 +/- 7)%, respectively. Pretreatment with GbE (10 mg x L(-1)) could not improve injured astrocytic glutamate response. But after pretreatment with GbE (100 mg x L(-1)), glutamate-induced [Ca2+]i elevation of astrocytes after hypoxia/reoxygenation, H2O2 or high concentration of L-glutamate injury were (135 +/- 98)%, (117 +/- 93)% and (89 +/- 36)%, respectively. Nimodipine (1.6 mg x L(-1)) could also reverse the abnormal response of astrocytes after different injury. CONCLUSION: Hypoxia/reoxygenation, H2O2 and high concentration of L-glutamate impaired astrocytes' response to exogenous L-glutamate, and then bidirectional communication between astrocytes and neurons could not take place. GbE could improve the abnormal responses and maintain the normal function of astroglical network. These effects support that GbE has potential beneficial actions against brain injury.


Assuntos
Astrócitos/metabolismo , Cálcio/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Ginkgo biloba , Animais , Astrócitos/citologia , Hipóxia Celular , Células Cultivadas , Córtex Cerebral/citologia , Córtex Cerebral/metabolismo , Medicamentos de Ervas Chinesas/isolamento & purificação , Ginkgo biloba/química , Ácido Glutâmico/toxicidade , Peróxido de Hidrogênio/toxicidade , Folhas de Planta/química , Plantas Medicinais/química , Ratos , Traumatismo por Reperfusão
11.
Yao Xue Xue Bao ; 40(10): 916-9, 2005 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-16408809

RESUMO

AIM: To observe the effect of phenolic alkaloids of Menispermum dauricum (PAMD) on thrombosis and platelet aggregation, and to explore its mechanism of action. METHODS: Thrombosis was observed with arteriovenous shunt thrombus model in rat; platelet aggregation was determined by Born's method; ultrastructure of platelet was observed by transmission electron microscope; TXB2 or 6-keto-PGF1alpha levels were assessed by radioimmunoassay; and NO was determined by colorimetric method. RESULTS: PAMD dose-dependently inhibited experimental thrombus formation, platelet aggregation induced by ADP, AA and THR in vivo and ultrastructure changes stimulated by THR; PAMD increased the generation of 6-keto-PGF1alpha in thoracic aortae and NO level in plasma; and had no influence on TXB2 release (P > 0.05). CONCLUSION: PAMD inhibited thrombosis and platelet aggregation, and its mechanism might be due to the increase of PGI2 and NO level.


Assuntos
Alcaloides/farmacologia , Benzilisoquinolinas/farmacologia , Menispermum , Agregação Plaquetária/efeitos dos fármacos , Tetra-Hidroisoquinolinas/farmacologia , Trombose/metabolismo , 6-Cetoprostaglandina F1 alfa/metabolismo , Alcaloides/administração & dosagem , Alcaloides/isolamento & purificação , Animais , Aorta Torácica/metabolismo , Benzilisoquinolinas/administração & dosagem , Benzilisoquinolinas/isolamento & purificação , Plaquetas/ultraestrutura , Relação Dose-Resposta a Droga , Epoprostenol/metabolismo , Masculino , Menispermum/química , Óxido Nítrico/sangue , Plantas Medicinais/química , Coelhos , Ratos , Ratos Sprague-Dawley , Rizoma/química , Tetra-Hidroisoquinolinas/administração & dosagem , Tetra-Hidroisoquinolinas/isolamento & purificação , Tromboxano B2/metabolismo
12.
Yao Xue Xue Bao ; 39(6): 401-5, 2004 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-15491093

RESUMO

AIM: To study the protective effect of procyanidins from the seedpod of the lotus (LSPC) on myocardial ischemia and reperfusion in rats. METHODS: Myocardial injury model was made by ligating the coronary artery for 30 min followed by reperfusion for 45 min in anesthetized rat and 30 min of ischemia followed by 30 min of reperfusion in the isolated rat heart. All animals were given the medicine or normal saline before the experiment. ET, Ang I, Ang II in the serum, the MDA content, SOD activity, NO level, the recovery rate of coronary flow (CF) and heart rate (HR) after reperfusion and CK, XO from the myocardial cells were observed. RESULTS: LSPC was shown to inhibit the release of ET, Ang II (P < 0.05) , and the increase of MDA content (P < 0.05). It was also found to increase the SOD activity (P < 0.05) and NO level (P < 0.01). LSPC was found to increase the recovery rate of the coronary flow (CF) and heart rate (HR) after reperfusion (P < 0.05 or P < 0.01), decrease the release of CK from the myocardial cells (P < 0.01), depress the XO activity of myocardial tissue (P < 0.05), as well as improve the myocyte ultrastructural pathological injury. CONCLUSION: The anti-ischemia effect of LSPC was related to the mechanism of scavenging the oxygen free radicals directly, cutting off the source of free radicals, reducing tissue peroxidation, stabilizing the cells membrane, depressing the production of EDCF and increasing the NO level as well.


Assuntos
Biflavonoides/farmacologia , Cardiotônicos/farmacologia , Catequina/farmacologia , Lotus/química , Isquemia Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Proantocianidinas/farmacologia , Animais , Biflavonoides/isolamento & purificação , Catequina/isolamento & purificação , Circulação Coronária/efeitos dos fármacos , Masculino , Isquemia Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Miocárdio/enzimologia , Miocárdio/ultraestrutura , Proantocianidinas/isolamento & purificação , Ratos , Ratos Wistar
13.
Yao Xue Xue Bao ; 38(9): 658-60, 2003 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-14730913

RESUMO

AIM: To observe the effect of phenolic alkaloids of Menispermum dauricum (PAMD) on the hemodynamics, coronary circulation and oxygen metabolism of the myocardium in anesthetized dogs. METHODS: In this study, the changes of LVSP, LVEDP and +/- dp/dtmax, the flow of coronary artery and myocardial energy metabolism were measured in anesthetized dog with PAMD or NS. RESULTS: In the anesthetized dogs, compared with pre-treatment status, PAMD at 3.5 and 7.0 mg.kg-1 caused decreases in the left ventricular systolic pressure(LVSP), +/- dp/dtmax, heart rate, the rate of oxygen utilization, the coronary and general peripheral resistance. It was found to increase myocardial oxygen and coronary flow. There were no significant change in the left ventricular end diastolic pressure (LVEDP). CONCLUSION: PAMD can ameliorate hemodynamics, coronary circulation and myocardial metabolism.


Assuntos
Alcaloides/farmacologia , Circulação Coronária/efeitos dos fármacos , Medicamentos de Ervas Chinesas/farmacologia , Menispermum/química , Alcaloides/isolamento & purificação , Animais , Pressão Sanguínea/efeitos dos fármacos , Débito Cardíaco/efeitos dos fármacos , Cães , Medicamentos de Ervas Chinesas/isolamento & purificação , Feminino , Frequência Cardíaca/efeitos dos fármacos , Masculino , Consumo de Oxigênio/efeitos dos fármacos , Plantas Medicinais/química , Distribuição Aleatória , Resistência Vascular/efeitos dos fármacos
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