Myocardial cell damage and breakdown of cation homeostasis during conditions of ischaemia and reperfusion, the oxygen paradox, and reduced extracellular calcium.

Enzyme release from perfused rat heart was determined under various conditions of injury. In analogous experiments, intracellular cation concentrations were measured using ion-selective microelectrodes. Under appropriate conditions, the inhibition of mitochondrial and/or glycolytic ATP production led to a decrease in the release of enzymes. During ischaemia or the oxygen paradox, the sarcosolic Ca2+ concentration was highly elevated; reperfusion or reoxygenation was followed by a drastic enzyme release. This was also found to be true under the conditions of an increased permeability brought about by a reduced extracellular Ca2+ concentration of 0.1 mmol/l. The intracellular pH under all conditions of injury was only moderately decreased. The sarcosolic Na+ concentration was markedly increased whereas the K+ concentration was decreased. The critical Ca2+ concentration of the sarcosol beyond which cell damage and enzyme release are inducible was assumed to be in the range between 10 and 32 mumol/l. The driving force of the Na+/Ca2+ exchange reaction of the sarcolemma is discussed in relation to recovery from hypoxic injury and the potential for avoiding cell damage.