The Effects Of Captopril Delayed Pretreatment On Caspase Expression Of VEC Induced By Hypoxia/Reoxygenation

The prevention and cure of ischemic/reperfusion injury has been become predominant topic in cardiovascular research domain.Ischemic preconditioning (IP)is the strongest protective mechanism and complicate cell defence phenomena in vivo.IP existence in not only organ level but also cell level.IP can ptrtect cardiomyocytes ,vascular smooth muscle cells or endothelial cells.The detect of IP established a new domain for protect ischemic myocardium and visit its mechanism.Previous research have been illustrated that hypoxia preconditioning and ischemic preconditioning had similar effects.Presenrly to practice injury preconditioning has been not accepted in clinic for it can produce damage.Now the research of induce preconditioning has transferred from ischemic,biologic,physics and chemistry to pharmalogical.Pharmalogical preconditioning bring about cardioprotective effect for excitaed or mimic endogenous materials. Angiotensin converting enzyme Inhibitor (ACEI) can produce pharmalogic preconditioning effect.It have been widely reported that ACEI induce or reinforce early cardioprotective effect,and few reported induce delay cardioprotective effect.Therefore,it is important to explore ACEI delay protective effect in endothial cell ischemic reperfusion(hypoxia/reoxygention) injury.and effect of Caspase 3.8.9 in endothial cell apoptosis by induced ischemic reperfusion. [objective] to detect ACEI delay protective effect in endothial cell ischemic reperfusion(hypoxia/reoxygention) injury.and effect of Caspase 3.8.9 in endothial cell apoptosis by induced ischemic reperfusion. [Methods] we created the ischemic reperfusion injury model for endothial cells. Catopril was applicated to experiment Human umbilical vein endothelial cells(HUVECS) were randomly divided into three groups by us : hypoxia/reoxygenation group were induced by hypoxia for 2...