Concern has often been expressed regarding the relevance of results from animals shocked with endotoxin and the human patient subjected to septic shock. The present study was designed to further test the animal model. Experiments were carried out on young adult baboons, lightly anesthetized, unrestrained, and separately subjected to 1-2 hr infusions of E. coli organisms (aver., 1010 org/kg) or E. coli endotoxin (aver., 25 mg/kg). Animals were found to be significantly more sensitive to E. coli than endotoxin on a canine-dose related basis. Similar responses in the two shock models were hepatic damage, including fibrin thrombi, central lobular congestion and/or hemorrhage, severe glycogen loss, marked mitochondrial swelling, dilatation and fragmentation of rough and smooth endoplasmic reticulum; greatly increased lactate, SGOT, LDH, and F-LDH values; pulmonary perivascular space edema, myocardial mitochondrial edema together with intra- and interfiber edema. The E. coli organism induced shock model was unique in that severe and sustained degrees of systemic hypotension with hypoglycemia and hypoinsulinemia were regularly observed; more notable pulmonary ultrastructural damage was seen; the consistent presence of renal fibrin thrombi was documented; and earlier deaths were recorded with E. coli than in the endotoxin model. Heparin administration (>2000 units/hr) prevented both the development of renal fibrin after E. coli and hepatic fibrin induced by endotoxin. Significant differences in the response to E. coli and endotoxin by the baboon suggest that uniquely complex differences elicited by separate mechanisms are operative in the two forms of shock.
|Original language||English (US)|
|Pages (from-to)||No. 108|
|Journal||Intensive care medicine|
|State||Published - Jan 1 1977|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine