Black S C, Driscoll E M, Lucchesi B R
Department of Pharmacology, University of Michigan Medical School, Ann Arbor, USA.
Pharmacology. 1998 Jul;57(1):35-46. doi: 10.1159/000028224.
Cardioprotective effects of the angiotensin-converting enzyme inhibitors captopril and ramiprilat were studied in two in vivo canine models of myocardial ischemic injury: 90 min of regional ischemia with 18 h reperfusion (protocol I) and 6 h of continuous ischemia without reperfusion (protocol II). In protocol I, neither ramiprilat (50 micrograms/kg) nor captopril (5 mg/kg + 0.25 mg/kg/h) reduced infarct size after 18 h of reperfusion (vs. controls). In protocol II, drugs were administered directly into both left anterior descending coronary artery and left circumflex branch. Compared to controls, continuous intracoronary administration of ramiprilat (40 ng/kg/min) or captopril (400 ng/kg/min) did not reduce infarct size. Thus neither captopril nor ramiprilat protected the heart from injury under conditions of ischemia with reperfusion or ischemia without reperfusion.
90分钟局部缺血并再灌注18小时(方案I)和持续缺血6小时且无再灌注(方案II)。在方案I中,再灌注18小时后,雷米普利拉(50微克/千克)和卡托普利(5毫克/千克 + 0.25毫克/千克/小时)均未减小梗死面积(与对照组相比)。在方案II中,将药物直接注入左冠状动脉前降支和左旋支。与对照组相比,冠状动脉内持续给予雷米普利拉(40纳克/千克/分钟)或卡托普利(400纳克/千克/分钟)并未减小梗死面积。因此,在有再灌注的缺血或无再灌注的缺血条件下,卡托普利和雷米普利拉均不能保护心脏免受损伤。