Phosphocreatine and adeninenucleotides in postasphyxial hearts with normal basal function and normal oxygen demand

Summary

We investigated whether there is a relationship between the prolonged dysfunction after myocardial ischaemia and the postischaemic phosphocreatine overshoot phenomenon. In 16 open-chest rats 3 periods of 4 minutes of oxygen deficiency were performed and basal haemodynamic variables and the myocardial oxygen demand were determined during the recovery period. At the end of the 20 minutes recovery period, left ventricular pressure, dp/dt_max, ejection fraction, and myocardial oxygen demand were completely recovered. High energy phosphate levels, however, were still altered. The sum of adeninenucleotides was decreased to 78 ± 4% of control ($(\overline x \pm$SEM, p<0.05) . The level of phosphocreatine was markedly elevated to 162 ± 14 ($(\overline x \pm$ SEM). The persistence of the phosphocreatine overshoot phenomenon, while basal function was already normalized, indicates that a reduced function and thus a reduced energy demand of the contractile apparatus are not the cause of the phosphocreatine overshoot. We found no close relationship between high energy levels and basal function or oxygen demand in myocardium after mild oxygen deficiency.

Supported by the Deutsche Forschungsgemeinschaft (Ho 1003/1-1).