Burn injury-induced nicotinic acetylcholine receptor changes on muscle membrane.

Patients with thermal injury show pharmacological responses akin to those seen following denervation of motor nerve where there is an increase in the number of muscle-type acetylcholine receptors (AChR). This study in the rat, examined the effect of 20%, 30%, and 50% body surface area burn injury on gastrocnemius and diaphragm AChR number, quantitated by [125I]alpha-bungarotoxin (alpha-BGT). Pharmacodynamic responses to D-tubocurarine were evaluated in the gastrocnemius muscle. AChR from gastrocnemius muscle were significantly increased in all burn groups at 14 days after burn. After 28 days, the AChR had returned to control in the 20% and 30% burn groups, but persisted in the 50% burn group. AChR from diaphragm did not show significant changes between groups. Resistance to D-tubocurarine was not seen in burn groups compared with controls. Burn trauma causes increases of AChR at sites distant from the area of injury. Diaphragm muscle may be less sensitive than gastrocnemius to mediators which upregulate AChR.