MYOCARDIAL PROTECTION IN NORMAL AND HYPOXICALLY STRESSED NEONATAL HEARTS - THE SUPERIORITY OF HYPOCALCEMIC VERSUS NORMOCALCEMIC BLOOD CARDIOPLEGIA

Objectives: The ideal cardioplegic calcium (Ca+2) concentration in new borns continues to be debated. Most studies examining cardioplegia cal cium concentrations have been done with a nonclinical model (i.e., iso lated heart preparation), the results of which may not be clinically a pplicable, and they have not examined the effect of calcium concentrat ion in a clinically relevant stressed (hypoxic) heart. Methods: Twenty neonatal piglets 5 to 18 days old were placed on cardiopulmonary bypa ss, and their aortas were crossclamped for 70 minutes with hypocalcemi c or normocalcemic multidose blood cardioplegic infusions. Group 1 (n = 5; low Ca+2, 0.2 to 0.4 mmol/L) and group 2 (It = 5; normal Ca+2, 1. 0 to 1.3 mmol/L) were nonhypoxic (uninjured) hearts. Ten other piglets were first ventilated at an Fio(2) of 8% to 10% (O-2 saturation 65% t o 70%) for 60 minutes (i.e., causing hypoxia) and then reoxygenated at an Fio(2) of 100% with cardiopulmonary bypass, which produces a clini cally relevant stress injury, They then underwent cardioplegic arrest (as described above) with a hypocalcemic (n = 5, group 3) or normocalc emic (it = 5, group 4) blood cardioplegic solution. Myocardial functio n was assessed with pressure volume loops and expressed as a percentag e of control values. Coronary vascular resistance was measured during each cardioplegic infusion. All values were reported as the mean +/- s tandard error. Results: In nonhypoxic hearts (groups 1 and 2), good my ocardial protection was achieved at either concentration of cardiopleg ia calcium, as demonstrated by preservation of postbypass systolic fun ction (104% vs 99% end-systolic elastance), minimally increased diasto lic stiffness (152% vs 162%), no difference in myocardial water (78.9% vs 78.9%), and no change in adenosine triphosphate levels or coronary vascular resistance. Low-calcium blood cardioplegia solution repaired the hypoxic reoxygenation injury in stressed hearts (group 3), result ing in no statistical difference in myocardial function, coronary vasc ular resistance, or adenosine triphosphate levels compared with nonhyp oxic hearts (groups 1 and 2). Conversely, when a normocalcemic cardiop legia solution was used in hypoxic hearts (group 4), there was marked reduction in postbypass systolic function (49% +/- 4% end-systolic ela stance; p < 0.05), increased diastolic stiffness (276% +/- 9%; p < 0.0 5), increased myocardial water (80.1% +/- 0.2%; p < 0.05), rise in cor onary vascular resistance (p < 0.05), and lower adenosine triphosphate levels compared with groups 1, 2, and 3. Conclusions: This study demo nstrates that, in the clinically relevant, intact animal model, good m yocardial protection is independent of cardioplegia calcium concentrat ion in nonhypoxic (noninjured) hearts; hypoxic (stressed) hearts are e xtremely sensitive to the cardioplegic calcium concentration; and norm ocalcemic cardioplegia is detrimental to neonatal myocardium subjected to a preoperative hypoxic stress.