Mechanism of Tracheal Constriction by Succinylcholine

Abstract
The mechanism by which succinylcholine produced large increases in endotracheal tube cuff pressure was studied in barbiturate-anesthetized dogs (n = 7). Cuff pressure was measured in vivo by a transducer connected to a fluid-filled, high-volume, low-pressure cuff. I.v. 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 1-3 min and declined slowly over the next 10 min. Bilateral vagotomy, i.v. 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 3 dogs were used to study the direct actions of succinylcholine on the trachealis muscle in vitro. In organ baths, succinylcholine (10-6 to 10-3 M) did not contract canine trachealis muscle, and concentrations .gtoreq. 10-15 M significantly relaxed carbamylcholine-induced contractions. Succinylcholine elicits contraction of the trachealis muscle by a stimulant action on parasympathetic pathways rather than by a direct action on airway smooth muscle. As vagotomy prevented the succinylcholine response, the site of stimulant action is not at autonomic ganglia.

This publication has 3 references indexed in Scilit: