Effect of rapid cooling contracture on ischemic tolerance in immature myocardium

Hypothermic perfusion before cardioplegic ischemic arrest is commonly used in neonatal cardiac surgery. However, perfusion cooling of the heart in the nonarrested state results in an inotropic response and may induce myocardial contracture secondary to a sustained elevation of intracellular calcium levels. The effect of prearrest cardiac cooling was examined in two groups of isolated parabiotic, blood-perfused neonatal rabbit hearts. Group C (cooling group, n = 12) was exposed to 15 minutes of cold perfusion to 12 degrees C before 1 hour of cardioplegic arrest. Group N (normothermia group, n = 11) underwent identical arrest conditions but without prearrest cold perfusion. Developed pressure at constant volume in group C fell from 109 +/- 8.7 mm Hg at baseline to 55.2 +/- 5.5 mm Hg after 30 minutes of reperfusion versus no significant change in group N. Diastolic compliance showed significant deterioration in group C, with marked elevation of diastolic pressure from 9.8 +/- 0.4 mm Hg at baseline to 22.0 +/- 4.4 mm Hg after ischemia and reperfusion. This experimental data demonstrates that profound hypothermic perfusion of the myocardium in the nonarrested state may induce a rise in resting myocardial tension and that cardioplegic ischemic arrest in the presence of cooling contracture may result in important myocardial injury.