We investigated the effect of two IV anesthetics, propofol and etomidate, on airway responsiveness in a rat model of chronic hypoxia (CH) in comparison with normoxic rats. CH rats were obtained using a hypobaric chamber (14 days at a barometric pressure of 380 mm Hg). The ability of both anesthetics to relax and prevent agonist-induced contraction was assessed in isolated tracheal rings precontracted with the muscarinic agonist carbachol (CCh) and the depolarizing agent KCl. Cumulative concentrations of both compounds relaxed tracheal rings precontracted with CCh or KCl with a similar amplitude in CH and normoxic rats. In tracheal rings precontracted with CCh, the negative logarithm of anesthetics that reduced the maximal contraction by 30%, i.e., -log half-maximal inhibitory concentration, for propofol and etomidate were 4.10 +/- 0.09 and 4.12 +/- 0.15 in normoxic rats and 4.20 +/- 0.22 and 3.61 +/- 0.19 in CH rats, respectively. At a fixed concentration, propofol (3 x 10(-4) M) or etomidate (10(-4) M) also inhibited CH tracheal rings contraction in response to cumulative concentrations of CCh and KCl. However, in contrast with the equivalent relaxant effect of both anesthetics, etomidate was two-fold less effective than propofol for inhibiting the subsequent contraction to CCh and KCl. These results indicate that propofol and etomidate retain their relaxant properties in CH rat airways by acting on the pharmaco- and electromechanical coupling.
Implications: Anesthesia may cause airway constriction or bronchospasm in patients with normal or pathological airways. This study investigated the ability of propofol and etomidate to both reverse precontraction and inhibit contraction of tracheal rings isolated from chronically hypoxic rats.