The relationship between myocardial enzyme release and Ca2+ uptake during hypoxia and reoxygenation in the newborn and adult heart.

The relationship between creatine phosphokinase (CPK) release and sarcolemmal permeability to divalent cations (Ca2+ and Ba2+) during hypoxia and reoxygenation was studied in the isolated arterially perfused septal preparation of the newborn and adult rabbit. Tissue 47Ca2+ or 133Ba2+ uptake was measured by a juxtaposed gamma-probe. Since Ba2+ is not taken up by the sarcoplasmic reticulum and mitochondria, 133Ba2+ was used to determine sarcolemmal permeability to divalent cations (Ca2+ and Ba2+). In the two age groups, tissue Ca2+ uptake was unchanged during hypoxia and increased significantly during reoxygenation. Ba2+ uptake remained unchanged during hypoxia and reoxygenation. CPK release was small during hypoxia and increased significantly during reoxygenation. The increases in tissue Ca2+ uptake and CPK release in the newborn were significantly less than in the adult. Perfusion with low Ca2+ solutions (0.3 mM, 0.5 mM and 'zero') decreased tissue Ca2+ gain but did not prevent CPK release during reoxygenation. In the muscle perfused with an oxygenated solution containing phospholipase C (0.1 U/ml), the rate of CPK release increased significantly, but tissue Ca2+ uptake and Ba2+ uptake remained unchanged. These data suggest that: (1) sarcolemmal damage (evidenced by enzyme release) during hypoxia and reoxygenation in the newborn is less than in the adult. (2) enzyme release and tissue Ca2+ gain can occur during reoxygenation without significant changes in sarcolemmal permeability to divalent cations (Ca2+ and Ba2+) that can be detected by the present techniques, and (3) enzyme release during reoxygenation is associated with but may not be caused by the increased tissue Ca2+.