Captopril cardioplegia on myocardial protection in the hypertrophied rat hearts.
Hearts with pressure-overload hypertrophy show an increased intracardiac activation of the renin-angiotensin system (RAS) which may contribute to myocardial ischemia and reperfusion injury. This study investigates whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and whether the specific inhibition of the cardiac RAS by captopril would modify ischemia and reperfusion injury in the hypertrophied myocardium. By using the isolated working rat heart model, hypertrophied hearts, induced by abdominal aortic banding for 6 weeks, were subjected to 120 min of hypothermic ischemic arrest followed by 30 min of reperfusion. The postischemic cardiac function recovery was measured in both the untreated (n = 10) and the captopril-treated (n = 11) groups and was compared with that of the sham-operated non-hypertrophied control hearts (n = 10). Captopril (23.0 microM) was given to one group with the hypertrophied hearts from the beginning of ischemia to the end of reperfusion. In comparison with the normal control hearts, the cardiac function recovery after 30 min reperfusion was poorer in the hypertrophied hearts, which was associated with a lower recovery of coronary flow (CF), a higher myocardial lactate content and a retarded peak myocardial creatinkinase (CK) release. Captopril significantly improved the cardiac function recovery, which was associated with an increased CF recovery and a lower myocardial lactate content, and a rapid peak CK release. In conclusion, this study shows that the hypertrophied myocardium leads to an increased susceptibility to ischemia and reperfusion injury. Captopril, most likely by its inhibition of the cardiac RAS, is effective in preventing the ischemia and reperfusion injury in the hypertrophied heart.
Zhang
Y H
YH
Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing.
Xu
S C
SC
D000818:Animals; D002216:Captopril / Q000627:therapeutic use*; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D006324:Heart Arrest, Induced; D017379:Hypertrophy, Left Ventricular / Q000150:complications*; D066298:In Vitro Techniques; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System; D016277:Ventricular Function, Left
D007773:Lactates; D019344:Lactic Acid; D002216:Captopril; D003402:Creatine Kinase