Succinylcholine potentiates responses to intravenous acetylcholine in the canine lung periphery

Abstract

Using the wedged bronchoscope technique to measure collateral resistance (Rcs), we evaluated the effect of succinylcholine (SCh) on the response to acetylcholine (ACh) and methacholine (MCh) in the lung periphery in six mongrel dogs. Dogs were anesthetized, intubated, and mechanically ventilated. After a stable baseline Rcs was obtained, responses to intravenous ACh (25-200 micrograms), intravenous MCh (3-30 micrograms), and aerosolized ACh (30-100 micrograms/ml for 15 s) were measured. We compared the Rcs responses with 1) ACh alone, 2) ACh 2 min after SCh (0.5 mg/kg), 3) ACh 2 min after SCh and during hexamethonium infusion (5 mg/kg + 10 mg.kg-1.h-1), 4) MCh 2 min after SCh, and 5) ACh aerosol 2 min after SCh. SCh did not significantly alter baseline airway tone. SCh increased the Rcs response to ACh by 48 +/- 17% (SE) (P less than 0.01). SCh in the presence of hexamethonium increased the Rcs response by 10 +/- 3% (P less than 0.05), while hexamethonium itself increased the response to ACh by 69 +/- 27%. Because SCh did not increase the Rcs response to intravenous MCh or to aerosolized ACh, SCh probably enhances airway reactivity to intravenous ACh by competing for pseudocholinesterase in plasma. We conclude that the level of muscle relaxant must be taken into account in interpreting studies of airway reactivity when intravenous ACh is employed.

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

“…Thus, they concluded that the tracheal contraction induced by SCh could result from stimulation of the parasympathetic nerves rather from than a direct action on the tracheal smooth muscle. Kaise et al [3], using a fi beroptic bronchoscope technique, showed that SCh increased the canine tracheal smooth muscle contraction induced by intravenous ACh, and that this increase was not completely abolished by hexamethonium. In addition, SCh did not increase the contraction induced by intravenous methacholine or aerosolized ACh.…”

“…Although succinylcholine (SCh) is often used as a muscle relaxant in ECT [1], its infl uence on airway reactivity has not been fully investigated. Kaise et al [3] studied a canine model, and reported that SCh probably enhanced airway reactivity to intravenous acetylcholine (ACh). Although the mechanism was not clear, they suggested that SCh might compete for plasma butyrylcholinesterase (BChE) against ACh, resulting in enhancement of ACh's action.…”

CHOLINESTERASE ACTIVITY IS SIMILAR IN C3H/HeJ AND A/J MICE AND DOES NOT ACCOUNT FOR THEIR DIFFERENT BRONCHOCONSTRICTOR RESPONSIVENESS

“…Previous studies have shown that cholinesterase enzymes found in the airways [5][6][7] and in the plasma [ 8] play an important role in regulating pulmonary function. Decreased cholinesterase activity is associated with both enhanced contractile responses of airway smooth muscle [ 5,6] and airway hyperresponsiveness [ 8] to acetylcholine.…”

“…Decreased cholinesterase activity is associated with both enhanced contractile responses of airway smooth muscle [ 5,6] and airway hyperresponsiveness [ 8] to acetylcholine.…”

“…Acetylcholinesterases and butyrylcholinesterases are present in the smooth muscle and ganglia of the rodent airway [ 6,13] and decreases in acetylcholinesterase [ 6,7,13] and butyrylcholinesterase [ 8] activities are associated with enhanced contractile responses to exogenous and endogenous acetylcholine. Although the acetylcholinesterase gene in the mouse has been localized to a chromosome that is not linked to airway hyperresponsiveness in mice ( chromosome 5) [ 14] , the chromosome location of the butyrylcholinesterase gene in the mouse has not yet been identi ed.…”