• S Magder and S Daniel.
• Critical Care Division, Royal Victoria Hospital, Montreal, Canada.
• J Crit Care. 1995 Dec 1; 10 (4): 174-82.

PurposeThis study was performed to determine the direct effect of endotoxin on force generation, O2 consumption and vascular resistance in contracting skeletal muscle.Materials And MethodsWe vascularly isolated the gastrocnemius muscle of dogs anesthetized with sodium pentobarbital and mechanically ventilated. The muscle was perfused from a proximal vessel or by a pump that withdrew blood from the contralateral leg. The nerve to the muscle was stimulated with supramaximal voltage 12 tr/min, 15-Hz impulses and a duty cycle of 0.4. Blood flow was measured with an electromagnetic flow probe, and oxygen consumption (VO2) was calculated from the flow and arterial-venous O2 content. In Protocol 1 (local infusion), contractions were stimulated for 30 minutes and endotoxin (n = 6) or saline (n = 6) was infused into the vasculature of the isolated gastrocnemius muscle after 10 minutes of contraction and continued for another 20 minutes of contraction. In Protocol 2 (systemic infusion), The normal tension and flow to the gastrocnemius were established and endotoxin (n = 5) or saline (n = 5) infused systemically. One hour later, the flow was set at the control level of contracting muscle, and contractions were stimulated for 30 minutes.ResultsIn both groups, endotoxin did not alter the tension VO2, arterial venous oxygen difference, or vascular resistance at the end of the stimulation period.ConclusionEndotoxin must affect muscle force production by acting through intermediates such as cytokines, and the effect is not apparent in the first 60 minutes.

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