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The paper summarizes the literature data and the authors' own investigations on cardiotropic and clinical-pharmacological properties of Mildronat. The medication normalizes energy metabolism, optimizes the functions of the heart, and improves the health state of patients with angina pectoris and cardiac insufficiency.

Intraperitoneal administration of pituitrin (2 units/kg) decreases the number of oxidized forms of nicotinamide coenzymes in the rat myocardium and raises the level of reduced forms and LDH activity. Nitroglycerin (1 mg/kg) prevents pituitrin-induced changes in the content of coenzymes and in LDH activity.

Examination of 94 patients with stage II hypertensive disease and 20 rabbits with hypertension showed that in the hypokinetic type of hemodynamics separate medication with dibazol, papaverin hydrochloride and reserpine caused a reduction of arterial pressure in all cases due to a decrease in total peripheral resistance. In combination with phentolamine dibazol and papaverin hydrochloride caused no further decrease of arterial pressure whereas the hypotensive effect of reserpine in this case was intensified along the type of summation of hypotensive effects due to more significant decrease in total peripheral resistance. During beta-adrenostructure blocking in patients with hyperkinetic type of hemodynamics, arterial pressure dropped due to a decrease of the cardiac output. Medication with dibazol, papaverin hydrochloride and reserpine during beta-adrenergic block led to more marked drop in arterial pressure because these agents prevented an increase of total peripheral resistance encountered when only beta-adrenergic blocking agents are given.

Alpha 1-adrenoceptor blocker--prazosin--was found to inhibit noradrenaline-induced depolarization and concentration in the smooth muscles of the portal rabbit vein, indicating that this reaction was due to alpha 1-adrenoceptor activation. In the pulmonary artery both alpha 1 and alpha 2-adrenoceptors appear to be involved in noradrenaline excitatory action, as the effect was not completely inhibited by prazosin. The results suggest that hypotensive action of prazosin is related to the cessation of Ca2+ ion influx through alpha 1-operated calcium channels. The decrease in Ca2+ influx through voltage-dependent calcium channels due to prazosin-evoked elimination of depolarization can also contribute to this effect.

Experimental thyrotoxicosis was induced in rats and rabbits. The content of catecholamines was significantly decreasing in the myocardium of rabbits in the presence of severe thyroidine-induced toxicosis. The noradrenaline concentration was especially low in the ventricles. The histochemical examination of the myocardium of rats revealed a reduction of catecholamines fluorescence, which indicates a decrease in their amount in the adrenergic structures.

The effects of dibasol on spontaneous electrical and contractile activities as well as on the reactions evoked by hyperkalemic solution and noradrenaline were studied in smooth muscle of rabbit portal vein. It was shown that dibasol blocked the potential-operated influx Ca2+ into smooth muscle cells. The noninactivating calcium channels were found to be more sensitive to dibasol than inactivating ones. Significant part of the tonic contraction induced by noradrenaline was resistant to dibasol suggesting its weak effect on Ca2+ influx through calcium channels operated by alpha 1-adrenoceptors. It is supposed that vasodilative effect of dibasol is associated with blocking the influx Ca2+ through potential-operated noninactivating calcium channels into smooth muscle cells.