Vascular endothelium in sepsis and endotoxemia.

Since septic or endotoxin shock was high mortality and morbidity, mechanisms for cardiovascular collapse have been intensely investigated. The vascular response to catecholamines and other agonists is greatly attenuated. The mechanisms are considered to be related to changes in endothelium function. The endothelium releases vasoconstrictor and vasodilator compounds. These autocoids normally interact with systemic and other local vascular controls, but during endotoxemia this balance is severely altered. Large artery endothelia are destroyed whereas the microvessels remain intact and functional. The release of nitric oxide, prostacyclin and endothelin is greatly enhanced. The cytokines from endotoxin seem, however, to be the major causal agents of the syndrome and affect the endothelial or receptors on the endothelia differentially, dependent on tissue location.