In experiments on guinea-pig isolated hearts, perfused under Langendorff preparation, it has been shown that heart volume load and inotropic stimulation were accompanied with an increase of nitric oxide synthesis (by 46 and 51% accordingly) and with a decrease in an oxygen cost of myocardial work. L-arginine or sodium nitroprusside administration resulted in a reduce of the oxygen consumption by 29% and a decrease of oxygen cost of myocardial work. Inhibition of NO-synthase activity lead to an opposite effect--an increase in both--O2 consumption and an oxygen cost of the heart work by 15 and 19%. The data obtained evidence that NO is a regulator of the oxygen consumption by tissues and it determines the oxygen cost of the myocardial work. Its lack can play an important role in the developing of pathological states of the cardiovascular system, which are followed with its insufficient synthesis.
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