OBJECTIVE: Monitoring of cardioplegia infusion pressure may be important, particularly in immature hearts and in hearts without coronary artery disease. We have investigated the effects of infusion pressure on the preservation of the isolated rat heart. METHODS: Hearts (five in each group) were subjected to a single (20 ml) infusion of St. Thomas' Hospital cardioplegic solution at pressures of 60, 120, 180 and 240 cmH2O (44-176 mmHg), followed by 30 min of hypothermic (20 degrees C) ischemia. RESULTS: Mean recovery of cardiac output (expressed as a percentage of its preischemic value) decreased with increasing infusion pressure: 96.1 +/- 0.6%, 87.3 +/- 2.1% (P < 0.05 vs. 60 cmH2O), 79.3 +/- 2.8% (P < 0.05 vs. 120 cmH2O), 72.0 +/- 3.0% (not significant vs. 180 cmH2O), respectively. Endothelial function, as assessed by pre- and post-ischemic ability to secrete NO in response to 5-hydroxytryptamine, remained relatively normal after infusion at 60 cmH2O, but changed from vasodilation to vasoconstriction after infusion at 240 cmH2O. Electron microscopy revealed mild endothelial damage after infusion at 240 cmH2O, which was greatly exacerbated by reperfusion and was accompanied by regions of myocyte damage compatible with reperfusion of unprotected myocardium. The relationship between cardioplegia infusion pressure and infusion time was not linear and implied that infusion pressures greater than 120 cmH2O caused vascular smooth muscle constriction. CONCLUSIONS: These results suggest that even mildly raised cardioplegia infusion pressures may be detrimental to cardiac preservation and the effects are possibly mediated through endothelial damage and pressure-induced coronary vasoconstriction.
OBJECTIVE: Monitoring of cardioplegia infusion pressure may be important, particularly in immature hearts and in hearts without coronary artery disease. We have investigated the effects of infusion pressure on the preservation of the isolated rat heart. METHODS: Hearts (five in each group) were subjected to a single (20 ml) infusion of St. Thomas' Hospital cardioplegic solution at pressures of 60, 120, 180 and 240 cmH2O (44-176 mmHg), followed by 30 min of hypothermic (20 degrees C) ischemia. RESULTS: Mean recovery of cardiac output (expressed as a percentage of its preischemic value) decreased with increasing infusion pressure: 96.1 +/- 0.6%, 87.3 +/- 2.1% (P < 0.05 vs. 60 cmH2O), 79.3 +/- 2.8% (P < 0.05 vs. 120 cmH2O), 72.0 +/- 3.0% (not significant vs. 180 cmH2O), respectively. Endothelial function, as assessed by pre- and post-ischemic ability to secrete NO in response to 5-hydroxytryptamine, remained relatively normal after infusion at 60 cmH2O, but changed from vasodilation to vasoconstriction after infusion at 240 cmH2O. Electron microscopy revealed mild endothelial damage after infusion at 240 cmH2O, which was greatly exacerbated by reperfusion and was accompanied by regions of myocyte damage compatible with reperfusion of unprotected myocardium. The relationship between cardioplegia infusion pressure and infusion time was not linear and implied that infusion pressures greater than 120 cmH2O caused vascular smooth muscle constriction. CONCLUSIONS: These results suggest that even mildly raised cardioplegia infusion pressures may be detrimental to cardiac preservation and the effects are possibly mediated through endothelial damage and pressure-induced coronary vasoconstriction.