The vascular abnormalities that arise during sepsis imply disturbances
in the delicately tuned homeostatic mechanisms of vascular endotheliu
m and smooth muscle. In the microvasculature, smooth muscle tone repre
sents a complex equilibrium among metabolic stimuli, hemodynamic force
s, and neurohumoral influences. Local tissue perfusion also is modulat
ed by vasoactive mediators that can be produced locally, through endot
helium-dependent adhesion and activation of inflammatory cells, or at
a distance. In sepsis, derangement of normal autoregulation of perfusi
on, together with toxic effects of mediators, may be severe enough to
result in organ dysfunction. Recent advances in vascular biology have
illuminated a variety of targets, such as adhesion molecules, platelet
activating factor, and inducible nitric oxide synthase for potential
therapeutic intervention in sepsis. Copyright (C) 1994 by W.B. Saunder
s Company