Effect of respiratory acidosis on hypoxic newborn myocardium

J Mol Cell Cardiol. 1989 Sep;21(9):927-34. doi: 10.1016/0022-2828(89)90760-8.


We studied the effect of respiratory acidosis (pH = 6.8) on mechanical function, tissue adenosine triphosphate (ATP), and effluent creatine kinase (CK) in isolated arterially perfused hypoxic newborn and adult rabbit hearts. In the oxygenated muscle, acidosis reduced tension (T) and maximal tension first derivative [+ dT/dt (max)] in the adult more than in the newborn. In the adult hypoxic and reoxygenated hearts, acidosis during hypoxia (not reoxygenation) improved the recovery of T, + dT/dt (max) and tissue adenosine triphosphate (ATP) and reduced CK release and the rise in the resting tension. In the newborn heart, respiratory acidosis during hypoxia had no beneficial effects on recovery of mechanical function, tissue ATP and CK release. The buffering capacity and sarcolemmal H-Na exchange rate are both higher in the newborn heart than in the adult heart. This suggests that acidosis reduces the rise in intracellular Na and Ca, that is observed during hypoxia and reoxygenation, in the adult more than in the newborn and this may explain the beneficial effect of acidosis in the adult and not in the newborn.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acidosis, Respiratory / physiopathology*
  • Adenosine Triphosphate / analysis
  • Age Factors
  • Animals
  • Animals, Newborn / physiology*
  • Asphyxia Neonatorum / physiopathology*
  • Creatine Kinase / analysis
  • Heart / drug effects
  • Heart / physiopathology*
  • Humans
  • Hypoxia / physiopathology*
  • Infant, Newborn
  • Myocardium / metabolism*
  • Oxygen / pharmacology
  • Phosphocreatine / analysis
  • Rabbits


  • Phosphocreatine
  • Adenosine Triphosphate
  • Creatine Kinase
  • Oxygen