Endotoxin-endothelium interactions in "low-perfusion state" research

LPS/endotoxin provokes a plethora of pathological events-Some of which may be considered as examples of "low perfusion state". These are discussed her e. It is well known that hypotension and refractoriness to vasocostrictors are the hallmark of endotoxic shock. Nevertheless, there are some vascular beds, such as mesenteric circulation, that respond with vasoconstriction - not: vasodilation to endotoxin. Aminoguanidine, an inhibitor of NOS-2, bloc ks endotoxin- induced increase of resistance in mesenteric bed and endotoxi n-induced translocation of bacteria through the gut wall. It is postulatede that endotoxin has antiarrythmogenic action due to the release of nitric o xide and increase in intracellular cGMP levels. Although we demonstrate tha t endotoxin increases nitric oxide formation in spleen and liver, its contr ibution to the injury of these organs by endotoxin is not fully established . In addition, we present our immunochemistry data on nitrotyrosine formati on in the liver and spleen of endotoxin-treated animals.