SUMMARY Twelve male neonatal calves (39 to 50 kg) were allotted to 3 groups of 4 calves each. All calves were anesthetized with halothane, and then Escherichia coli endotoxin was given intravenously (3 times) and intraperitoneally (3 times) during a 6-hour period. Group-1 calves were untreated, group-2 calves were pretreated with a low dose of flunixin meglumine (1.1 mg/kg of body weight), and group-3 calves were pretreated with a high dose of flunixin meglumine (4.4 mg/kg). In calves of group 1, the mean systemic arterial blood pressure ( mabp ) and cardiac output ( co ) decreased, but pulmonary arterial pressure increased after the initial intravenous and intraperitoneal injections of endotoxin. In calves of this group, these changes were accompanied by increased plasma thromboxane B 2 (TxB 2 ) concentration. During this period, increased plasma TxB 2 concentration or hemodynamic changes were not detected in calves of groups 2 and 3. Only calves of group 1 had altered hemodynamics early in the experiment; however, after 6 hours, calves of all 3 groups had similarly decreased co and mabp. In calves of the untreated group, plasma 6-keto-prostaglandin ( pg )F 1α concentration increased steadily from the beginning of the experiment until 3 hours later. The co and mabp were low at the time when serum 6-keto- pgf 1α concentration was high; however, these 2 measurements also were low in treated calves who did not have correspondingly high plasma 6-keto pgf 1α concentration. Regional blood flow analysis did not reveal correlations between prostanoid concentrations and altered blood flow to selected tissues. Results indicated that endotoxin given to calves caused increases in plasma TxB 2 and 6-keto- pgf 1α concentrations, along with hemodynamic changes similar to those observed in other species. Flunixin meglumine (1.1 mg/kg) administration prevented the increase in plasma eicosanoid concentrations and the associated hemodynamic changes during early shock. However, in treated calves, after 3 hours, the co and mabp also were decreased without a corresponding increase of plasma 6-keto- pgf 1α concentration. Therefore, something other than increased prostacyclin accumulation may have caused the later decrease in co and mabp.
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Templeton et al. (1988) studied this question.
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