摘要
实验研究血管紧张素转换酶抑制剂（ＡＣＥＩ）赖诺普利和卡托普利对离体大鼠心脏缺血再灌损伤的保护作用。结扎大鼠冠状动脉左前降枝１５ｍｉｎ，以造成大鼠心脏缺血再灌，赖诺普利（０．１μｍｏｌ／Ｌ）和卡托普利（２００μｍｏｌ／Ｌ）明显减少了缺血再灌所致室颤的发生。两种ＡＣＥＩｓ还抑制缺血１５ｍｉｎ分别再灌１和５ｍｉｎＬａｎｇｅｎｄｏｒｆｆ大鼠心脏去甲肾上腺素（ＮＡ）的释放，同时也降低了缺血再灌大鼠心脏钙离子的浓度。卡托普利（２００μｍｏｌ／Ｌ）不仅降低了缺血１５ｍｉｎ再灌５ｍｉｎ大鼠心脏自由基的浓度，还能清除由光照核黄素所产生的超氧阴离子，抑制率分别为２８．８０％和４１．６４％。而赖诺普利对自由基无任何影响。结果表明赖诺普利和卡托普利均能减少缺血再灌对心肌的损伤作用。这种作用可能是抑制了ＮＡ的释放，和降低钙离子浓度有关。赖诺普利无自由基清除作用可能是因其分子结构中不含巯基，卡托普利含巯基所致。
The effects of the angiotensin converting enzyme inhibitors (ACEI) captopril and lisinopil on injury induced by ischemia/reperfusion were investigated in the isolated working heart and Langendorff perfused rat heart. Ischemia/reperfusion was produced by ligation of the left descending branch of the coronary artery for 15 minutes followed by reperfusion for 1 or 5 minutes.The high doses of captopril (200 μmol/L) and lisinopril (0. 1μmol/L) reduced the incidence of ventricular fibrillation following ischemia/reperffusion in both working and Langendorrff perfused hearts. Furthermore,both ACEI (captopril. 200 μmol/L ;lisinopril,0. 1 μmol/) attenuated the myocardial noradrenalin and calcium concentration following ischemia/reperfusion in Langendorff perfused hearts.In contrast,only captopril reduced the formation of free fadicals following ischemia.reperfusion in Langendorff perfused hearts. Also the formation of superoxide anion in vitro by UV irradiation of a riboflavin/DMPO mixture was only diminished by captopril.We conclude that both captopril and lisinopril protect the myocardium against injury induced by ischemia/reperfusion.The beneficial effects of captopril probably depend on scavenging of free radicals and on prevention of calcinm overload and noradrenalin release,whereas the beneficial effects of lisinopril probably only depends on prevention of calium overload and noradrenalin relese induced by ischemia/reperfusion.
出处
《中华高血压杂志》
CAS
CSCD
1994年第4期232-236,共5页
Chinese Journal of Hypertension
