title: Endothelial and vascular smooth muscle function in sepsis.
abstract: The vascular abnormalities that arise during sepsis imply disturbances in the delicately tuned homeostatic mechanisms of vascular endothelium and smooth muscle. In the microvasculature, smooth muscle tone represents a complex equilibrium among metabolic stimuli, hemodynamic forces, and neurohumoral influences. Local tissue perfusion also is modulated by vasoactive mediators that can be produced locally, through endothelium-dependent adhesion and activation of inflammatory cells, or at a distance. In sepsis, derangement of normal autoregulation of perfusion, 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.
authors.affiliation: Division of Cardiology, Rush-Presbyterian-St Luke's Medical Center, Chicago, Illinois.
authors.forename: S M
authors.initials: SM
authors.lastname: Hollenberg
authors.forename: R E
authors.initials: RE
authors.lastname: Cunnion
mesh_terms: D004730:Endothelium, Vascular / Q000502:physiology / Q000503:physiopathology*; D006439:Hemodynamics; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology / Q000503:physiopathology*; D012772:Shock, Septic / Q000097:blood / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000378:metabolism; D014665:Vasodilator Agents / Q000378:metabolism
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents