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To study the relative roles of creatine kinase (CK) and adenylate systems in cardiac energy turnover, the effect of CK inhibitor, iodoacetamide- (IAA, 0.5 mM), and 2-deoxyglucose-(DOG, 2 mM) induced) 65% depletion of adenine nucleotides at slightly decreased CK flux was determined in isolated rat heart. Both substances did not substantially affect contractile parameters of the isovolumic heart. However, an augmentation of cardiac work induced by isoproterenol addition was feeble and transient in IAA-treated hearts while the response of DOG-treated hearts was well preserved. The cardiac failure after IAA treatment was associated with irreversible fall in myocardial ATP content as evidenced by 31P-NMR technique. Furthermore, these hearts were unable to perform cardiac pump function due to insufficient cardiac filling and distensibility. The DOG-treated hearts exhibited 50% reduction in the pump function and were able to increase their work in elevated resistance. The results suggest that CK pathway is extremely important for both full cardiac relaxation and maximal contractile function.

The combined effect of glutamic acid (15 mM) and phosphocreatine (10 mM) on metabolism and postischemic recovery of cardiac function was studied in isolated perfused working guinea pig hearts. Addition of these two agents into standard hyperpotassium cardioplegic solution increased twice the recovery of the aortic output and improved restoration of volume work and an index of functional recovery. This effect was combined with the complete recovery of ATP, phosphocreatine, the decrease in ammonia and lactate tissue contents and preservation of amino acid pool. Lesser leakage of creatine and creatine kinase pointed to lesser damage of the sarcolemma. The results show the effectiveness of the use of cardioplegic solution containing both glutamic acid and phosphocreatine.

It is shown that in rabbits subjected to an electric stimulation of the aortic arch there developed concurrently with depletion of tissular norepinephrine reserves in the myocardium also gross metabolic disorders. A preliminary introduction of the drug izm-611 by blocking central alpha-adrenoreseptors at the same time prevented depletion of the tissular norepinephrine reserves and development of disturbances of the energy exchange in the myocardium caused by its neurogenic damage.

The effect of aethimizol, introduced to rabbits before and after inflicting a 3-hours long extraordinary stimulation applied to the reflexogenic zone of the aortic arch, was studied. Investigations covered some aspects of energy metabolism and the level of the norepinephrine mediator in the muscle of the heart and also the functional state of the latter. Aethimizol was found to prevent shifts of the studied metabolic factors, induced by electric stimulation, and also to avert depletion of norepinephrine in the tissue of the myocardium and normalize its function.

A total of 92 patients with chronic tonsilitis and cardiovascular changes were subjected to clinical observations, ECG analysis, potassium and nitroglycerine tests, and studies of the lactic acid level and creatinekinase activity as indces of myocardial metabolism. The examinations were conducted prior to and following tonsillectomy. In a majority of patients a correlation was revealed between the degree of ECG changes and the serum lactic acid level, as well as between the ECG improvement and a reduction of the lactic acid level following tonsillectomy. Three stages of tonsillogenic myocardiodystrophy were distinguished. The obtained data indicate the rationale of the used tests for the evaluation of the myocardial meabolism alterations and of the efficacy of treatment of chronic tonsillitis patients.

Neurogenic damage of the myocardium by electrostimulation of the aortic arch led to deficiency of tissue noradrenaline (the sympathetic nervous system mediator). Simultaneously there was a marked rise of the glucose-6-phosphate dehydrogenase activity. Preliminary administration of the RNA synthesis inhibitor--actinomycin D--fully prevented the increase of this enzyme activity in the myocardium produced by its neurogenic damage. The data obtained testified to the acceleration of induction of this enzyme in the myocardium in case of its neurogenic damage, this correlating with the change of tissue noradrenaline balance.

In acute experiments on rats adapted for 4 weeks to the altitude of 2100 m it was found that at the early period of altitude adaptation the left ventricular systolic pressure and the maximal rates of pressure rise and fall considerably exceeded the values of control tests conducted in Moscow. Later on the parameters of the cardiac contractile function stabilized gradually. In 4 weeks the heart of adapted animals showed a greater increment of the contractility parameters in response to noradrenaline injection and a higher stability of the contractile function at very high heart rates.

A comparison was conducted between the contractile function of the heart of hares and rabbits at rest and under isometric contractions regimens, and under such conditions the concentration of ATP and its breakdown products was studied in the myocardium of both species. It was demonstrated that the cardiac muscle of hares adapted by the evolution to the performance of intensive work does not possess any increased ability of developing systolic tensions, or any increased power of the ATP resynthesis apparatus. The advantage of such a heart-- its ability to pump an increased blood volume -- must be ensured by some different mechanism that requires still further investigations.

Male albino rats were adapted to 6 km "altitude" in barocamber. Responses of their hearts in open chest and on artificial respiration to noradrenaline and propranolol were studied. Values of the heart contractory function were by 32-140% higher in experimental animals than in control those. This excess could be eliminated by propranolol which shows it to be due to exaggerated effect of the adrenergic regulatory link. Adrenaline raises the heart function almost up to the maximal limit in adapted animals. This is followed by an increased rate of disappearance of the noradrenaline inotropic effect.

The pump function of the isolated rat or guinea pig hearts was assessed at various functional loads. The diastolic left ventricular (LV) stiffness was determined by a ratio of a rise in LV pressure for a diastole to LV filling volume for a diastole. This index was several times lower for guinea pig's hearts as compared to the rat hearts at equal heart rate. It was associated with a higher cardiac output of guinea pig hearts at low left atrium filling pressure. The rat hearts, however, having a higher diastolic stiffness adapted better to increased resistance or elevated heart rate, preserved the cardiac output and markedly increased cardiac work. The data obtained suggest that LV diastolic stiffness is an important factor determining cardiac adaptation to various functional loads; its influence seems to be actualized through changes in the LV filling.