Pathogenesis of lethal shock after intravenous staphylococcal enterotoxin B in monkeys.
The pathogenesis of shock in the rhesus monkey given intravenous staphylococcal enterotoxin B (SEB) is not understood. Several cardiovascular changes produced by a highly purified preparation of SEB were studied after administration of doses ranging from 50 to 1,000 mug/kg. Irreversible arterial hypotension was found consistently at the higher doses. Arterial blood pressure and cardiac output declined substantially as shock developed. Total peripheral vascular resistance did not rise at any time, but showed a significant fall during the late stages of shock. Portal and central venous pressures remained essentially unchanged. Venous O(2) content and pO(2) declined gradually throughout the period of toxemia, but arterial O(2) content remained constant until just prior to death, when a slight fall was noted in some monkeys. These changes were consistent with a pooling of blood in the peripheral vascular beds and seemed to resemble cardiovascular responses reported to occur in monkeys during shock due to bacterial endotoxin. Epinephrine, administered in the late stages of shock, caused arterial pressure to increase almost immediately and cardiac output to return to normal about 1 min later. Although life could occasionally be prolonged for several hours by continuous or intermittent epinephrine infusions, this therapy never succeeded in reversing the lethal effects of high doses of SEB.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D002339:Carotid Arteries; D004768:Enterotoxins; D004837:Epinephrine / Q000494:pharmacology; D000882:Haplorhini; D010100:Oxygen / Q000097:blood; D012039:Regional Blood Flow; D012772:Shock, Septic / Q000503:physiopathology*; D013210:Staphylococcus
D004768:Enterotoxins; D010100:Oxygen; D004837:Epinephrine