PROTECTIVE EFFECT OF NITRIC-OXIDE DURING HEAT-SHOCK

Hyperproduction of the endogenous vasodilator nitric oxide (NO) is a m ain cause of arterial pressure during shocks of various origin. Here w e show that the introduction of an exogenous NO donor, dinitrosyl iron complexes, reliably decreases mortality in rats due to heat shock fro m 57% to 8%. Simultaneously, dinitrosyl iron complexes prevent acute h ypotension, excessive inhibition of vasoconstrictory, and enhancement of vasodilatory reactions related to NO hyperproduction. We propose th at the protective effect of exogenous NO is due to inhibition of exces sive synthesis of endogenous NO according to the negative feedback mec hanism. Since dinitrosyl iron complex is a compound in which endogenou s NO is deposited in the body under natural conditions, this NO donor is a promising means of prevention and therapy of pathological states related to both NO efficiency and hyperproduction.