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.