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 here. 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, blocks endotoxin- induced increase of resistance in mesenteric bed and endotoxin-induced translocation of bacteria through the gut wall. It is postulatede that endotoxin has antiarrythmogenic action due to the release of nitric oxide and increase in intracellular cGMP levels. Although we demonstrate that endotoxin increases nitric oxide formation in spleen and liver, its contribution to the injury of these organs by endotoxin is not fully established. In addition, we present our immunochemistry data on nitrotyrosine formation in the liver and spleen of endotoxin-treated animals.
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Department of Pharmacology Faculty of Medicine, Hacettepe University, Ankara, Turkey.
D000758:Anesthesia; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology*; D004731:Endotoxins / Q000633:toxicity*; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D009569:Nitric Oxide / Q000009:adverse effects / Q000096:biosynthesis*; D013154:Spleen / Q000378:metabolism* / Q000473:pathology; D014443:Tyrosine / Q000031:analogs & derivatives / Q000096:biosynthesis
D004731:Endotoxins; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; D003907:Dexamethasone