Effect of ACE inhibitor captopril and L-arginine on the metabolism and on ischemia-reperfusion injury of the isolated rat heart

We investigated the effects of in vivo treatment with the angiotensin-conve rting enzyme inhibitor (ACE-I) captopril and/or of in vitro administration of L-arginine on the metabolism and ischemia-reperfusion injury of the isol ated perfused rat myocardium. Captopril (50 mg/l in drinking water, 4 weeks ) raised the myocardial content of glycogen. After 25-min global ischemia, captopril treatment, compared with the controls, resulted in lower rates of lactate dehydrogenase release during reperfusion (8.58 +/-1.12 vs. 13.39 /-1.88 U/heart/30 min, p<0.05), lower myocardial lactate contents (11.34<pl us/minus>0.93 vs. 21.22 +/-4.28 mu mol/g d.w., p<0.05) and higher coronary flow recovery (by 25 %), and prevented the decrease of NO release into the perfusate during reperfusion. In control hearts L-arginine added to the per fusate (1 mmol/l) 10 min before ischemia had no effect on the parameters ev aluated under our experimental conditions, presumably because of sufficient saturation of the myocardium with L-arginine. In the hearts of captopril-t reated rats, L-arginine further increased NO production during reperfusion and the cGMP content before ischemia. Our results have shown that long-term captopril treatment increases the energy potential and has a beneficial ef fect on tolerance of the isolated heart to ischemia. L-arginine added into the perfusate potentiates the effect of captopril on the NO signaling pathw ay.