PATHOGENESIS OF EXPERIMENTAL SHOCK

Abstract

Donor rabbits were subjected to shock by occlusion of the superior mesenteric artery (SMAO shock). Portal blood was collected from these animals at certain intervals after release of the arterial ligature. Infusion of this blood into sub-lethally hemorrhaged rabbits caused the death of half of the tested animals; a mortality incidence which closely matched the per cent mortality in rabbits shocked by SMA occlusion alone. Blood from sham-operated donor animals did not prove lethal when infused into hemorrhage-prepared rabbits. Infusion of SMAO shock plasma did not result in the death of recipient animals, even though the whole blood source of the plasma had proven to be lethal upon infusion into hemorrhage-prepared rabbits. Moreover, following pretreatment of donor animals with a non-absorbable antibiotic per os, the number of actively reproducing bacteria in the intestinal fluids was reduced to less than 0.1 per cent of normal; nevertheless, the incidence of passive transfer of lethality from shocked donors receiving this pretreatment was not consistently reduced. Furthermore, when SMAO shock portal blood was tested for the presence of bacterial endotoxin by the sensitive dermal epinephrine reaction, although some blood samples demonstrated lesion-provoking activity, there was no correlation between this activity and the lethal properties of the blood samples. In seeking an explanation for the production of dermal epinephrine lesions by non-lethal shock blood, a positive correlation was demonstrated between the lesion-provoking activity of portal blood and the serotonin content of intestinal tissues of rabbits shocked by SMA ligation. In addition, small amounts of serotonin were shown to be capable of provoking dermal epinephrine reactions in rabbits, under the same conditions used to test the lesion-provoking activity of portal blood. It was therefore concluded that: (a) a toxic factor(s) is present in the portal blood of SMAO-shocked rabbits; (b) that this factor(s) is not likely to be a bacterial endotoxin; and (c) that the occasional provocation of a dermal epinephrine reaction by portal blood from SMAO-shocked rabbits, a property heretofore exclusively attributed to the presence of endotoxin in shock blood, can be entirely explained on the basis of elevated levels of serotonin in this blood.