INFLUENCE OF THE PH OF CARDIOPLEGIC SOLUTIONS ON CELLULAR-ENERGY METABOLISM AND HYDROGEN-ION FLUX DURING NEONATAL HYPOTHERMIC CIRCULATORY ARREST AND REPERFUSION - A DYNAMIC P-31 NUCLEAR-MAGNETIC-RESONANCE STUDY IN A PIG MODEL

Objectives: The pH of cardioplegic solutions is postulated to affect m yocardial protection during neonatal hypothermic circulatory arrest, N either optimization of cardioplegic pH nor its influence on intracellu lar pH during hypothermic circulatory arrest has been previously studi ed in vivo, Thus we examined the effects of the pH of cardioplegic sol utions on postischemic cardiac function in vivo, including two possibl e operative mechanisms: (1) reduction in adenosine triphosphate use an d depletion of high-energy phosphate stores or (2) reduction of H+ flu x during reperfusion, or both, Methods: Dynamic P-31 spectroscopy was used to measure rates of adenosine triphosphate use, high-energy phosp hate depletion, cytosolic acidification during hypothermic circulatory arrest, and phosphocreatine repletion and realkalinization during rep erfusion. Neonatal pigs in three groups (n = 8 each)-group A, acidic c ardioplegia (pH = 6.8); group B, basic cardioplegia (pH = 7.8); and gr oup N, no cardioplegia-underwent hypothermia at 20 degrees C with 60 m inutes of hypothermic cardioplegia followed by reperfusion, Results: R ecoveries of peak elastance, stroke work, and diastolic stiffness were superior in group B, Indices of ischemic adenosine triphosphate use, initial phosphocreatine depletion rate, and tau the exponential decay half-time, were not different among groups, Peak [H+] in group A (end- ischemia) was significantly elevated over that of group B, The realkal inization rate was reduced in group B compared with that in groups A ( p = 0.015) and N (p = 0.035), with no difference between groups A and N (p = 0.3), Cytosolic realkalinization rate was markedly reduced and the half-time of [H+] decay was increased during reperfusion in group B, Conclusions: Superior postischemic cardiac function in group B is n ot related to alterations in ischemic adenosine triphosphate use or hi gh-energy store depletion, but may be due to slowing in H+ efflux duri ng reperfusion, which should reduce Ca++ and Na+ influx.