Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury.

摘要: 1. Coronary artery reperfusion has become the treatment of choice for evolving myocardial infarction. 2. While there is no question that timely restoration coronary blood flow essential salvage ischaemic myocardium, also been associated with potentially deleterious consequences. Specifically, viable tissue salvaged by remains 'stunned'--i.e., exhibits prolonged abnormalities in contractile function--for hours to days following reflow. Furthermore, it suggested per se may lethally injure some myocytes were only reversibly injured prior flow. 3. ACE inhibitors such as captopril and enalapril have shown reduce indices injury (infarct size, creatine kinase release) enhance function stunned myocardium experimental models occlusion followed reperfusion. These effects largely attributed reduction O2-demand increase blunting angiotensin II formation. 4. Recent studies suggest inhibitors--particularly captopril--may not solely be explained on basis inhibition. In fact, sulphydryl (-SH) containing appear act scavengers oxygen-derived free radical species thought important pathogenesis both postischaemic dysfunction ischaemia/reperfusion induced myocyte necrosis. 5. Thus, -SH inhibitors--which inhibit scavenge cytotoxic radicals--may offer a suitable form injury.