Succinylcholine potentiates acetylcholine-induced contractile and phosphatidylinositol responses of rat trachea

Although succinylcholine (SCh) is often used as a muscle relaxant in electroconvulsive therapy, its influence on airway reactivity has not been fully investigated. We examined the effects of SCh on acetylcholine (ACh)-, carbachol (CCh)-, and electrical field stimulation (EFS)-induced contractions, and on the ACh-induced phosphatidylinositol (PI) response of rat trachea.

Thirty-two male Wistar rats weighing 250-350 g were used. The trachea was rapidly isolated and cut into 3-mm-wide rings. The resting tension was adjusted periodically to 1.0 g during the equilibration period. ACh, 1 microM; carbachol (CCh), 0.05 microM; or neither of them, was added, and SCh was then added at 1-300 microM final concentrations, and ring tension was examined. Contractions were elicited by EFS in the presence or absence of 100 microM SCh. Tracheal slices were incubated with [3H] myo-inositol, 1 microM ACh, and various concentrations of SCh. The accumulation of [3H] inositol monophosphate (IP1) was measured.

SCh did not affect the tension by itself without ACh, or with CCh, but SCh potentiated the ACh-induced contraction of rat trachea at concentrations of 10 microM or more (50% effective concentration [EC50]; 43.6 microM). SCh produced a significant increase in the amplitude and duration of EFS-induced contractions. SCh, at concentrations of 10 microM and 100 microM, potentiated ACh-induced IP1 accumulation.

SCh potentiated ACh-induced, but not CCh-induced, contractile and PI responses, and enhanced EFS-induced contraction of rat trachea, suggesting that competition for butyrylcholinesterase (BChE) in airway smooth muscle could be involved in the potentiation by SCh of ACh-induced airway smooth muscle contraction.