Mechanism of tracheal constriction by succinylcholine.
The purpose of this study was to identify the mechanism by which succinylcholine produced large increases in endotracheal tube cuff pressure in barbiturate-anesthetized dogs (n = 7). Cuff pressure was measured in vivo by a transducer connected to a fluidfilled, high-volume, low-pressure cuff. Intravenous succinylcholine, 0.5 and 1 mg/kg, produced mean increases in cuff pressure of 12 +/- 2 (+/-SE) and 27 +/- 5 cm H2O, respectively, which reached peak effect in 1 to 3 min and declined slowly over the next 10 min. Bilateral vagotomy, intravenous administration of atropine (0.2 mg/kg) and hexamethonium (5 mg/kg) prevented or terminated succinylcholine-induced increases in cuff pressure. Isolated preparations from an additional three dogs were employed to study the direct actions of succinylcholine on trachealis muscle in vitro. In organ baths, succinylcholine (10(-6) to 10(-3) M) did not contract canine trachealis muscle, and concentrations of 10(-5) M and above significantly relaxed carbamylcholine-induced contractions. The authors conclude that succinylcholine elicits contraction of trachealis muscle by a stimulant action on parasympathetic pathways rather than by a direct action on airway smooth muscle. Since vagotomy prevented the succinylcholine response, the site of stimulant action is not at autonomic ganglia.[1]References
- Mechanism of tracheal constriction by succinylcholine. Koga, Y., Downes, H., Leon, D.A., Hirshman, C.A. Anesthesiology (1981) [Pubmed]
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