Thermal injury results in dystropic changes in skeletal muscle and abnormal pharmacological responses to neuromuscular relaxants, each of which suggests a denervation-like phenomenon. In the rat thermal injury model we examined whether, as in denervation states, increases in nicotinic acetylcholine receptors (AChR) and hyposensitivity to d-tubocurarine (dTc) are found. While anesthetized, thermal injury was imposed to trunk only. At 10, 14, and 21 days after injury the effective doses of dTc for left gastrocnemius tension suppression to 95% of control tension (ED95) were 0.213 +/- 0.039, 0.305 +/- 0.070, and 0.214 +/- 0.032 mg/kg, respectively. These values were significantly higher (P less than 0.05) than control values (0.155 +/- 0.006 mg/kg). The AChR concentrations in the left gastrocnemius, quantitated by 125I-alpha-bungarotoxin binding, increased at 10, 14, and 21 days to 182 +/- 20% (P less than 0.001), 166 +/- 22% (P less than 0.03), and 164 +/- 18% (P less than 0.001) of control, respectively. AChR concentrations in the right gastrocnemius also increased subsequent to thermal injury. Changes in effective dose of dTc for 50 and 95% twitch suppression in the left gastrocnemius correlated significantly with changes in AChR concentrations for the same muscle (r = 0.73 and 0.81, P less than 0.001, respectively). This study confirms the hypothesis that the systemic effects of thermal injury include an increase in AChR at sites distant from thermal injury, which may account for the skeletal muscle dysfunction and aberrant responses to neuromuscular relaxants.

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