The effect of halothane on the steady-state levels of high-energy phosphates in the neonatal heart.
The neonatal heart is especially vulnerable to cardiac depression caused by halothane. The cause of this sensitivity is uncertain. Isolated, perfused, isovolumic, contracting neonatal rabbit hearts were studied using 31P NMR to determine whether changes in concentrations of high energy phosphates (HEP) or intracellular pH mediated the effects of halothane. Steady-state HEP concentrations and intracellular pH were unaffected, despite profound reductions of mechanical performance. The data also suggest that halothane, in the concentrations studied, does not cause significant uncoupling of oxidative phosphorylation.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D003864:Depression, Chemical; D006221:Halothane / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006863:Hydrogen-Ion Concentration; D007424:Intracellular Fluid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010710:Phosphates / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism*; D011817:Rabbits
D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006221:Halothane