Effect of cardioplegia infusion pressure on coronary artery endothelium and cardiac mechanical function

OBJECTIVE: Monitoring of cardioplegia infusion pressure may beimportant, particularly in immature hearts and in hearts without coronaryartery disease. We have investigated the effects of infusion pressure onthe preservation of the isolated rat heart. METHODS: Hearts (five in eachgroup) were subjected to a single (20 ml) infusion of St. Thomas' Hospitalcardioplegic solution at pressures of 60, 120, 180 and 240 cmH2O (44-176mmHg), followed by 30 min of hypothermic (20 degrees C) ischemia. RESULTS:Mean recovery of cardiac output (expressed as a percentage of itspreischemic 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 < 0.05vs. 120 cmH2O), 72.0 +/- 3.0% (not significant vs. 180 cmH2O),respectively. Endothelial function, as assessed by pre- and post-ischemicability to secrete NO in response to 5-hydroxytryptamine, remainedrelatively normal after infusion at 60 cmH2O, but changed from vasodilationto vasoconstriction after infusion at 240 cmH2O. Electron microscopyrevealed mild endothelial damage after infusion at 240 cmH2O, which wasgreatly exacerbated by reperfusion and was accompanied by regions ofmyocyte damage compatible with reperfusion of unprotected myocardium. Therelationship between cardioplegia infusion pressure and infusion time wasnot linear and implied that infusion pressures greater than 120 cmH2Ocaused vascular smooth muscle constriction. CONCLUSIONS: These resultssuggest that even mildly raised cardioplegia infusion pressures may bedetrimental to cardiac preservation and the effects are possibly mediatedthrough endothelial damage and pressure- induced coronaryvasoconstriction.