Effect of captopril cardioplegia on renin-angiotensin system, prostaglandins, free radicals and electrolytes in the isolated hypothermic ischemic and reperfusion rabbit hearts

The effect of captopril cardioplegia on ischemic and reperfusion myocardium after 3 hours of hypothermic (13 +/- 1 C) arrest and 35 minutes of reperfusion was studied in the isolated working rabbit heart. In comparison with the control group, captopril cardioplegia reduced the content of angiotensin II (381 +/- 56 vs 507 +/- 84 pg/g wt of the control group, P < 0.01) and MDA (50.0 +/- 9.2 vs 85.1 +/- 16.1 pmol/mg pr, P < 0.01) in the reperfusion myocardium; augmented the renin activity of ischemic (1050 +/- 353 vs 669 +/- 301 pg/g wt/h, P < 0.05) and reperfusion myocardium (1261 +/- 421 vs 498 +/- 353 pg/g wt/h, P < 0.01) increased the 6-K-PGF1 alpha/TXB2 ratio in the reperfusion myocardium (by 48.1% of the control group). Meanwhile, captopril cardioplegia could also decrease the content of calcium (0.027 +/- 0.015 vs 0.045 +/- 0.014 microM/mg pr, P < 0.05) and sodium (0.54 +/- 0.26 vs 0.82 +/- 0.15 microM/mg pr, P < 0.05) in the reperfusion myocardium, but had no effect on the potassium content. The results show that the protective effect of captopril on hypothermic myocardium may be related to the free radical scavenging action, inhibition of angiotensin II production, improvement of PGI2/TXA2 ratio and decrease of calcium and sodium overload in the myocardium.