Burn Injury to Rat Increases Nicotinic Acetylcholine Receptors in the Diaphragm

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Abstract
Thermal injury induces aberrant responses to neuromuscular (NM) blocking drugs, and it has been speculated that an increase in nicotinic acetylcholine receptors (AchR) may contribute to the altered response. Using the diaphragmatic muscle as a representative of skeletal muscle, the changes in AchR were examined. The diaphragm, rather than limb muscles, was chosen to avoid the effects of wound contracture-induced immobilization and denervation of limb, which can also increase AchR in skeletal muscle. Study of changes in diaphragm also tested the hypothesis that increase in AchR are the result of a generalized systemic effect, and not limited to area of burn. Following a 45-55% body surface area thermal injury to the trunk (not limbs) of rats, AchR changes in the diaphragm were studied at 10, 14, 21, and 28 days after injury and compared to uninjured (control) rats. The AchR changes in the diaphragmatic muscle was assayed using 125I-alpha-bungarotoxin as the specific ligand. At 10, 14, and 21 days after thermal injury, the animals had an arrest in weight growth and the AchR concentration was increased to (mean .+-. SE) 155 .+-. 15% (P < 0.02), 160 .+-. 16% (P < 0.003), and 141 .+-. 16% (0.05 < P < 0.1), respectively, compared to control. At 28 days, probably because of wound healing and burn wound contracture, the size of thermally injured area was significantly (P < 0.001) reduced to 19 .+-. 4% of body surface area, and weight increased (P < 0.001) compared to preburn weight. The AchR number at 28 days after burn returned to control levels (111 .+-. 14% of control, P < 0.6). Thus major thermal injury causes significant increases in AchR at sites distant from burn, which revert to normal with decrease in size of the injured area.