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- W1972473400 abstract "The initial responses to endotoxemia are detectable in the microcirculation as a microvascular inflammatory response characterized by activation of the endothelium stimulating these cells from their normal anticoagulant state to a procoagulant state with increased adhesiveness for leukocytes and platelets. Concomitantly, arteriolar tone is lost and reactivity to a variety of agonists is modified. Tissue damage subsequently results not only from reduced perfusion of the exchange vessels, but also from injurious substances released from activated, sequestered leukocytes as well as activated endothelial cells, macrophages, and platelets. This is the result of endotoxins inducing activation and interaction of a number of effector cells, cascades, and acute-phase responses, such as the complement, coagulation, bradykinin/kinin, and hematopoietic systems accompanied by the release of a myriad of mediators. These include eicosanoids, cytokines, chemokines, adhesion molecules, reactive free radicals, platelet-activating factor, and nitric oxide. This paper briefly reviews the microvascular responses to endotoxemia and discusses some of the mechanisms involved." @default.
- W1972473400 created "2016-06-24" @default.
- W1972473400 creator A5046452074 @default.
- W1972473400 creator A5079413998 @default.
- W1972473400 creator A5085407899 @default.
- W1972473400 date "1996-10-01" @default.
- W1972473400 modified "2023-09-26" @default.
- W1972473400 title "The microcirculation during endotoxemia" @default.
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