Coronary endothelial injury by cold crystalloid cardioplegic solution in neonatal lambs

Hypothermic cardioplegia generally improves the recovery of the mechanical function of the heart after ischemia, but some components of cold cardioplegia may produce endothelial injury that can offset the protective effects of cardioplegia. This study was undertaken to evaluate the effect of extremely hypothermic cardioplegia on the recovery of coronary endothelial and cardiac mechanical function after ischemia in the immature heart.

Three groups of eight isolated, blood-perfused, neonatal lamb hearts each had myocardial temperature maintained at 10 degrees C during 2 hours of global ischemia but received hourly doses of crystalloid cardioplegic solution at temperatures of 10 degrees C (group A), 4 degrees C (group B), and 2 degrees C (group C). The percent recovery of isovolumic left ventricular maximum developed pressure in groups A (86.6 +/- 7.7) and B (90.5 +/- 7.5) was higher than in group C (78.6 +/- 6.3), and maximum dP/dt in groups A (89.6 +/- 8.6) and B (89.5 +/- 5.7) was higher than in group C (79.4 +/- 9.0) at 30 minutes of reperfusion (p < 0.05). Groups A (136.8 +/- 20.9) and B (142.8 +/- 27.7) achieved higher recovery of coronary blood flow (as percentage of baseline) at 15-minute reperfusion than group C (108.5 +/- 26.2), and myocardial oxygen consumption was higher in groups A (68.3 +/- 14.6, 92.1 +/- 21.1) and B (68.8 +/- 19.9, 85.3 +/- 25.5) than in group C (46.3 +/- 14.7, 57.2 +/- 14.2) at 15 and 30 minutes of reperfusion, respectively (p < 0.05). Percent recovery of the coronary vascular resistance responses to 10(-7) M concentration of an endothelium-dependent vasodilator (acetylcholine) in groups A (71.9 +/- 9.0) and B (66.2 +/- 23.1) was higher than in group C (24.2 +/- 14.3) (p < 0.05), whereas responses to 3 x 10(-5) M concentration of endothelium-independent vasodilator (nitroglycerin) were the same.

Excessively cold cardioplegic solution may cause endothelial dysfunction (reduced acetylcholine response) and reduced recovery of mechanical function in the neonatal heart.