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A study was conducted to examine if endothelial cell dysfunction initially takes place during hemorrhage, and in case of this dysfunction taking place, to examine if it continues after fluid resuscitation in a nonheparinized model of trauma-hemorrhage and resuscitation. Rats were bled and kept at mean arterial pressure of 40 mm Hg till 40% maximal bleed-out volume was given back in the form of Ringer lactate. During the maximal bleed-out time, there was lowered loosening and contraction, depending on endothelium which continued despite crystalloid resuscitation following hemorrhage.

Hepatocellular dysfunction and enhanced tumor necrosis factor (TNF) in hyperdynamic sepsis were analysed using intravenous introduction of recombinant murine TNF-alpha. Hepatic microcirculation was unaffected by TNF-alpha-created hepatocellular dysfunction. No relation was observed between hepatocellular dysfunction and other hemodynamic parameters. TNF-stimulation individually or in combination with interleukin-6 was believed to be chiefly responsible for hepatocellular dysfunction.