Manukhina E B, Pokidyshev D A, Maleniuk E B, Malyshev I Iu, Vanin A F
Izv Akad Nauk Ser Biol. 1997 Jan-Feb(1):54-8.
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.
内源性血管扩张剂一氧化氮（NO）的过度产生是各种原因引起休克时动脉血压变化的主要原因。在此我们表明，引入外源性NO供体二亚硝基铁配合物，可使热休克大鼠的死亡率从57%可靠地降低至8%。同时，二亚硝基铁配合物可预防急性低血压、过度抑制血管收缩以及增强与NO过度产生相关的血管舒张反应。我们认为，外源性NO的保护作用是由于根据负反馈机制抑制了内源性NO的过度合成。由于二亚硝基铁配合物是一种在自然条件下内源性NO可在体内沉积的化合物，这种NO供体是预防和治疗与NO效能和过度产生相关病理状态的一种有前景的手段。
