The role of cardioplegia induction temperature and amino acid enrichment in neonatal myocardial protection

Background. Warm cardioplegic induction improves the ischemically "stressed " adult heart. However, it is rarely used in infants, despite the fact that many newborn hearts are stressed by other factors such as hypoxia. The nee d for amino acids as well as their mechanism of action has also not been st udied. Methods. We first assessed the role of cardioplegic induction temperature i n 10 nonhypoxic neonatal piglets undergoing 70 minutes of multidose blood c ardioplegic arrest. Five piglets (group 1) received a cold (4 degrees C) in duction, and 5 (group 2) a warm (37 degrees C) induction. Twenty-six other piglets underwent ventilator hypoxia (fraction of inspired oxygen, 8% to 10 %) for 60 minutes before cardiopulmonary bypass (stress). Six piglets (grou p 3) then underwent 70 minutes of cardiopulmonary bypass without ischemia ( hypoxia controls), and 20 underwent 70 minutes of cardioplegic arrest. Five of these (group 4) received cold cardioplegic induction, and 15 received w arm induction; in 5 of these (group 5), the warm cardioplegic solution cont ained amino acids, in 5 others (group 6), it was unsupplemented, and in the remaining 5 (group 7), nitroglycerin was added to determine the role of va sodilation. Myocardial function was assessed by pressure-volume loops (expr essed as a percent of control), and coronary vascular resistance was measur ed with cardioplegic infusions. Results. In nonhypoxic (normal) piglets, cold (group 1) and warm (group 2) induction completely preserved systolic function (end-systolic elastance, 1 00% versus 104%) and preload recruitable stroke work (100% versus 102%), wi th minimal increase in diastolic compliance (162% versus 156%). Hypoxia-reo xygenation alone (group 3) depressed systolic function (end-systolic elasta nce, 51% +/- 2%) and preload recruitable stroke work (54% +/- 3%), and rais ed diastolic stiffness (260% +/- 15%). The detrimental effects of reoxygena tion persisted (unchanged from reoxygenation alone) with cold induction (gr oup 3) or warm induction without amino acids (groups 6 and 7). In contrast, warm induction with amino acids (group 5) restored systolic function (end- systolic elastance, 105% +/- 3%; p < 0.001 versus groups 3, 4, 6, and 7) an d preload recruitable stroke work (103% +/- 2%; p < 0.001 versus groups 3, 4, 6, and 7), and decreased diastolic stiffness (154% +/- 79/0; p < 0.001 v ersus groups 3, 4, 6, and 7). However, there was no difference in myocardia l oxygen consumption in hypoxic hearts receiving a warm induction (6.9 vers us 6.5 versus 7.3 mL/g per 5 minutes) (groups 5, 6, 7), and coronary vascul ar resistance was lowest with nitroglycerin (group 7). Conclusions. Cardioplegic induction can be given either warm or cold in non hypoxic neonatal hearts. In contrast, only warm induction with amino acids repairs the hypoxic injury, but the primary mechanism of action is not rela ted to increased metabolic activity or vasodilation. (Ann Thorac Surg 2000; 70:756-64) (C) 2000 by The Society of Thoracic Surgeons.