Postischemic reperfusion injury and endotoxemia have been shown to promote multiple organ failure in polytraumatized patients. Both pathomechanisms comprise endothelial injury, leukocyte activation, and enhanced leukocyte/endothelium interaction in the microcirculation. Using a dorsal skinfold chamber model for intravital microscopy in striated muscle of awake hamsters, we investigated whether acute endotoxemia enhances postischemic leukocyte/endothelium interaction. - In control animals (n = 8), reperfusion after 2 hours of pressure induced ischemia elicited the rolling and adhesion of fluorescently stained leukocytes to the endothelium of postcapillary venules with a maximum at 0.5 and 2 hours after reperfusion and a decline towards preischemic values after 24 hours. Postischemic leukocyte adhesion was enhanced and protracted in animals where acute endotoxemia was induced through intravenous injection of endotoxin (Salmonella abortus equi, 0.1 microg¿kg superset-1) either 10 minutes prior to ischemia (n = 8) or to reperfusion (n = 8). - These results suggest that acute endotoxemia has the potential to aggravate the leukocyte-triggered reperfusion damage to striated muscle and presumably to vital organs and thus favours the development of multiple organ failure after primarily successful reperfusion.