Alterations in neuromuscular function following thermal injury.

Severe burn injury can result in dramatic changes in human physiology and biochemistry. Aberrant responses, hypersensitivity and potentially lethal hyperkalemia to depolarising [1,2] and hyposensitivity to non-depolarising [2,3] muscle relaxants have been noted in burn trauma. The molecular basis of these responses is currently thought to be due to an increase in nicotinic acetylcholine receptors in skeletal muscle [4,5]. Using a rat thermal injury model [4,5], we investigated the effect of three sizes of thermal injury, 20, 30 and 50% burn at 10, 14, 21 and 28 days post burn on:1)the pharmacodynamics of d-tubocurarine in evoked twitch (tension) responses of the left gastrocnemius muscle mediated via the sciatic nerve [41 2)an alteration in receptor number reflected by changes in [125I] ui-bungarotoxin binding to receptors from individual diaphragm and gastrocnemius muscles, extracted essentially as described [6] with filtration binding using the cationic polymer polyethylenimine [71.