[Oxidative damage to the myocardium: the protective action of exogenous phosphocreatine].

Oxidative damage of the isolated perfused rat heart was caused by addition of 90 microM H2O into Krebs-Henseleit solution. After 20 min of H2O2 addition an elevation of diastolic pressure (irreversible contracture) was observed followed by decrease of developed tension and heart work. Addition of phosphocreatine (10 mM) at constant total sodium concentration prevented the development of contracture and diminished the decrease of cardiac work.

[High specificity in the molecular mechanism of the protective action of phosphocreatine on the myocardium in ischemia].

To study the character of the mechanism of protective action of phosphocreatine on ischemic myocardium the effects of phosphocreatine (PCr) and phosphoarginine (PArg) were compared. PCr and PArg were shown to expose identical Ca2+-chelating properties and were used as their Na-salts. Only PCr protected the cardia function during ischemia and simultaneously inhibited the accumulation of lysophosphoglycerides, products of phospholipid degradation.

Protection of ischemic myocardium by exogenous phosphocreatine. II. Clinical, ultrastructural, and biochemical evaluations.

In valve replacement operations on 78 patients with acquired heart disease, the efficiency of phosphocreatine in intraoperative protection of ischemic myocardium was evaluated by clinical, morphologic, and biochemical methods. Phosphocreatine (8 to 10 mmol/L) in a blood cardioplegic solution was used in operations on 41 patients; in the control group (37 patients) standard blood cardioplegia was used. In the group with phosphocreatine treatment we observed more rapid recovery of hemodynamics after release of the aortic cross-clamp, a decreased frequency of fibrillation, and more frequent restoration of sinus rhythm even if there were sinus rhythm disturbances before aortic cross-clamping.

[Pharmacokinetics of phosphocreatine in the blood serum of man, dogs and rabbits].

It is shown that a single intravenous injection of phosphocreatine to man or to experimental animals is followed by its rapid clearance from blood serum. This clearance is biphasic in nature with a half-life of 3-5 min at the first rapid stage and of 20-33 min at the next slower stage. To maintain the constant phosphocreatine concentration in blood, it is necessary to infuse it at a rate comparable to that of clearance.