RESUMO
Accumulating evidence indicates that oxymatrine may exert protective effects on the cardiovascular system. This study was designed to evaluate the antiarrhythmic effects as well as the electrophysiological properties of oxymatrine. The antiarrhythmic activity of oxymatrine was observed in a rat model of arrhythmia induced by coronary ligation. Action potential duration (APD), L-type calcium current (I(Ca-L) ), transient outward potassium current (I(to) ) and inward rectifier potassium current (I(K1)) in rat ventricular myocytes were recorded by utilizing the whole cell patch-clamp technique. The results showed that administration of oxymatrine significantly delayed the onset of ventricular arrhythmia, decreased the duration of ventricular arrhythmia and reduced the arrhythmia score of arrhythmic rats. The beneficial effects of oxymatrine may be related to the shortening of APD through reduction of I(Ca-L) , enhancement of I(to) and inhibition of I(K1).
Assuntos
Alcaloides/farmacologia , Antiarrítmicos/farmacologia , Arritmias Cardíacas/tratamento farmacológico , Miócitos Cardíacos/efeitos dos fármacos , Quinolizinas/farmacologia , Sophora/química , Potenciais de Ação/efeitos dos fármacos , Animais , Arritmias Cardíacas/fisiopatologia , Canais de Cálcio Tipo L/efeitos dos fármacos , Técnicas Eletrofisiológicas Cardíacas , Masculino , Técnicas de Patch-Clamp , Canais de Potássio Corretores do Fluxo de Internalização/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
Microvessel hypoperfusion following ischemic stress resulted in a decreased shear stress of brain microvascular endothelial cells (BMECs) and contributed to abnormal expression of PECAM-1 after global cerebral ischemia/reperfusion (I/R) injury. Here, we identified novel pathophysiologic and rehabilitative procedures specific to shear stress in microvascular endothelial cells in response to global cerebral I/R injury. We found that the decrease in cerebral blood flow of gerbils after global cerebral I/R injury reduces shear stress, and the abnormal change in shear stress leads to microvascular endothelial cell and neuron damage. Nevertheless, suitable high levels of shear stress contribute to rescuing the dysfunction and malformation of BMECs via regulating the PECAM-1-eNOS-NO pathway to enhance nitric oxide release, decrease the expression of caspase-3 to reduce apoptosis, and improve the shear-adaptability of endothelial cells, thereby playing a protective role in the gerbil brain.