THE MICROCIRCULATION DURING ENDOTOXEMIA

The initial responses to endotoxemia are detectable in the microcircul ation as a microvascular inflammatory response characterized by activa tion of the endothelium stimulating these cells from their normal anti coagulant state to a procoagulant state with increased adhesiveness fo r leukocytes and platelets. Concomitantly, arteriolar tone is lost and reactivity to a variety of agonists is modified. Tissue damage subseq uently results not only from reduced perfusion of the exchange vessels , but also from injurious substances released from activated, sequeste red leukocytes as well as activated endothelial cells, macrophages, an d platelets. This is the result of endotoxins inducing activation and interaction of a number of effector cells, cascades, and acute-phase r esponses, such as the complement, coagulation, bradykinin/kinin, and h ematopoietic systems accompanied by the release of a myriad of mediato rs. These include eicosanoids, cytokines, chemokines, adhesion molecul es, reactive free radicals, platelet-activating factor, and nitric oxi de. This paper briefly reviews the microvascular responses to endotoxe mia and discusses some of the mechanisms involved.