Role of nitric oxide in hemorrhagic shock

It is stated in this article that the free radical nitric oxide is synthesized from enzymes termed the constitutive and inducible NO synthase and cellular intoxication of NO as well as the pathophysiology of hemorrhagic shock in relating to NO. Recent studies suggest that NO is responsible to irreversible from reversible shock owing to adhesion of PMN in the vascular endothelium. Insufficiency of the vascular endothelium loses ability of vasodilatation in brain, kidney, coronary vessels. The mechanism of vascular inability is not clarified yet, but PAF may be involved in. No produced from constitutive NOS prevents adhesion of PMN as well as platelet and produces vasodilatation. NO produced from inducible NOS observed in the late stage of hemorrhagic shock induces cytotoxic effects and leads to circulatory decompensation. Inducible NOS suppresses cardiac muscles and the injuries are prevented by L-NMMA or dexamethasone. Finally NOS inhibitors and NO related to traumatic, anaphylactic, and thermal injury are stated.