[The protective effect of nitric oxide in heat shock]

Hyperproduction of the endogenous vasodilator nitric oxide (NO) is a main cause of arterial pressure during shocks of various origin. Here we show that the introduction of an exogenous NO donor, dinitrosyl iron complexes, reliably decreases mortality in rats due to heat shock from 57% to 8%. Simultaneously, dinitrosyl iron complexes prevent acute hypotension, excessive inhibition of vasoconstrictory, and enhancement of vasodilatory reactions related to NO hyperproduction. We propose that the protective effect of exogenous NO is due to inhibition of excessive synthesis of endogenous NO according to the negative feedback mechanism. Since dinitrosyl iron complex is a compound in which endogenous 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.