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Early myocardial dysfunction induced with endotoxin in rhesus monkeys.

The effects of endotoxemia on basic cardiovascular function were examined in the in situ hearts of five anesthetized rhesus monkeys. Cardiovascular function was assessed by each heart's ability to maintain sufficient oxygen delivery, as measured by the reduction-oxidation state of cytochrome aa3 during periods of increased work and decreased oxygen availability. In addition, the effects of endotoxemia on the baroreflex loop were tested by infusion of the alpha-agonist phenylephrine (5 micrograms/kg). Finally, the oxidative capacity of heart mitochondria, isolated 4 h after the infusion of endotoxin, was determined. Immediately following the 30 min intravenous infusion of endotoxin (10 mg/kg), there was a reduction of cytochrome aa3 evident in the paced heart (200 beats/min) exposed to a brief hypoxic episode. This reduction indicates a loss of the ability of the heart to adjust oxygen delivery to the metabolic needs of the subepicardium. The pressor response to phenylephrine was also affected immediately following infusion, decreasing to 14.5 +/- 9.2% of control at 4 h. The chronotropic response to phenylephrine, mediated by the baroreceptor reflex, was reduced at t = 30 mins and was essentially abolished 3 h after infusion. There was no diminution of the oxidative capacity of the isolated mitochondria. These data indicate that endotoxemia has early depressive effects on the cardiovascular system in nonhuman primates.