Key messages

• Oxidation is the major factor producing endothelial barrier damage.

• Oxygen radicals are associated with activation, rolling adherence, and transmigration of leukocytes at endothelial barriers.

• Ischemia-reperfusion injury involves neutrophils and communication between these cells, the endothelium, and surrounding parenchymal cells.

• Endotoxin damage is a longer inflammatory response associated with cytokine release by macrophages and plasma cells and their subsequent effect on the endothelial barrier.

• Tumor necrosis factor and interleukin 1 are cytokines required to produce endothelial damage associated with sepsis and ischemia-reperfusion.

• Cell cAMP levels modify endothelial barrier integrity by controlling the tension in the actin-myosin light-chain complex inside the endothelial cell relative to their effects on intracellular junction size.

• Specific antibodies against various cytokines, leukocyte adherence and rolling factors, and intracellular mechanisms responsible for producing damage in plasma and endothelial cells will be important treatment tools in the critically ill.

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