Antioxidants for the treatment of endothelial dysfunction in critical illness

Abstract

Before 1980, the endothelium was considered to be an inert hemostatic barrier. Furchgott and Zawadzki were the first to demonstrate the necessity of the vascular endothelium for vasodilatation to acetylcholine [1]. If the vascular endothelium was removed, the blood vessel failed to relax in response to acetylcholine, but still responded to glyceryl trinitrate. This endothelium-dependent vaso dilatation is mediated by an endogenous mediator, initially named endothelium-derived relaxing factor (EDRF), but which was subsequently identified as nitric oxide (NO). From this discovery a new era of endothelial research developed. The endothelium is now known to have a key role in the maintenance of vascular homeostasis. It actively regulates vascular tone, platelet aggregation, coagulation, fibrinolysis, and leukocyte activation [2]. Endothelial function is impaired in critical illness and may be important in the pathophysiology of multiple organ failure (MOF) [3]. © 2007 Springer Science + Business Media Inc.