Enterotoxic shock in rhesus monkeys. The role of selected bloodborne factors.

Staphylococcal enterotoxin B, a protein exotoxin from Staphylococcus aureus, produced progressive hypotension and shock when injected (1 mg/kg, iv) into rhesus monkeys. Plasma levels of factors which have been implicated in the pathogenesis of other types of shock were measured. Endotoxin-like activity was measured by the Limulus lysate technique, fibrin degradation products (FDP) were quantified by electroimmunoassay, and activation of the complement system was assayed by measuring total hemolytic complement. Activation of the intrinsic coagulation cascade was assessed by measuring activated partial thromboplastin time (APTT). Activation of the kinin system was evaluated by measuring prekallikrein activity and kininogen. Myocardial depressant factor (MDF) was measured by paper chromatography. Endotoxin-like activity did not appear in plasma, and the complement system was not activated. The appearance of FDP and a significant trend for prolongation of APTT indicated activation of fibrinolysis and the intrinsic coagulation cascade, and suggested that disseminated intravascular coagulation was occurring. Activation of the kinin system was shown by a progressive and significant depletion of kininogen from 338 ± 37 to 226 ± 22 ng kallidin generated/ml, and a significant depletion of plasma prekallikrein activity from 169 ± 8 to 110 ± 15 tosyl arginine methyl ester (TAMe) esterase U/ml. Analysis of covariance indicated that activation of the kinin system was related to changes in blood pressure. MDF did not increase until immediately before death (increase from 1.08 ± 0.15 to 1.92 ± 0.11 paper chromatographic U//tl, n = 6). We conclude that kinins, MDF, and disseminated intravascular coagulation, but not complement or endotoxin, may contribute to the pathogenesis of enterotoxic shock in rhesus monkeys.