Nitric oxide and circulatory shock

Abstract

Since the discovery of nitric oxide, there has been significant progress in our understanding of its biosynthesis and its numerous biological actions in both health and disease. Knowledge about its role in shock syndrome is also accumulating rapidly. Excessive production of nitric oxide by iNOS and inhibition of NO generation by ecNOS appear to contribute in a significant way to progressive decrease in blood pressure, occurrence of thrombosis and vascular hyporeactivity, myocardial depression, tissue damage and eventual death due to endotoxemia. Excessive NO may contribute to various other forms of circulatory shock as well. From a therapeutic point of view, selective inhibition of iNOS, with concomitant upregulation of ecNOS (e.g., by 17β- estradiol) may offer significant clinical benefits in these diseases.