Previous investigators have shown that intravenous infusion of partially purified urinary callicrein would reproduce the many features of the shock syndrome. However, infusion of either pancreatic or urinary callicrein prepared by an ethanolic fractionation procedure failed to kill the dogs even when it was given in amounts nine times that previously reported to be toxic. Investigations directed towards the identification of the toxin as measured by earlier studies suggested that a combination of endotoxin and callicrein may have been responsible for the reported lethality. Callicrein is presumed to exert its hypotensive effect by enzymatic action on callidinogen, present in normal plasma, by effecting the release of a polypeptide called callidin. Measurement of the callidinogen content of plasma of dogs killed with endotoxin or by irreversible hemorrhagic shock indicated that small amounts of callicrein may have been released and that these quantities might thus contribute to the death of the animal. The possible synergistic effect and relationship between endotoxin, callicrein and plasmin are discussed.
Ubiquinol decreases hemorrhagic shock/resuscitation-induced microvascular inflammation in rat mesenteric microcirculation
