THE INFLUENCE OF SYMPATHOADRENAL ACTIVATION ON SKELETAL-MUSCLE OXYGENEXTRACTION DURING ENDOTOXEMIA

We have previously shown a direct relationship (r = .97) between the f all in arterial blood pressure and the increase in skeletal muscle oxy gen extraction (MVO2) during canine endotoxemia. Since it is well know n that hypotension activates the sympathetic system, the primary aim o f these experiments was to determine if the increase in MVO2 during en dotoxemia is a result of elevated levels of catecholamines due to incr eased sympathetic neural and/or humoral activity (sympathoadrenal syst em). Canine gracilis muscles were vascularly isolated and perfused in situ at a constant flow (6-7 ml/min/100 g). Endotoxemia was induced by a 30 min intravenous infusion of Escherichia coli endotoxin (2 mg/kg) , which induced a 50% reduction in arterial pressure. Perfusion pressu re, mean arterial pressure, and arteriovenous oxygen difference (a-v O 2) were continuously measured. We found 1) no significant difference b etween the amount of O2 extracted by an innervated or a denervated mus cle during endotoxemia; 2) the intra-arterial infusion of norepinephri ne or epinephrine into a denervated gracilis muscle (plasma molar conc entrations of; 10(-11), 10(-9), 10(-7), and 10(-5) failed to increase MVO2 to the level observed during endotoxemia; 3) pretreatment of a mu scle with propranolol to block skeletal muscle beta-adrenergic recepto rs, did not suppress the endotoxin-induced rise in MVO2. We concluded that the increase in MVO2 seen after the administration of endotoxin i s not due to either increased sympathetic nerve activity or elevated l evels of circulating catecholamines. We speculate that the increased M VO2 during endotoxemia is caused by nonadrenergic mediators released b y endotoxin rather than the hypotensive stimulus.