Low-temperature modification of the inhibitory effects of volatile anesthetics on airway smooth muscle contraction in dogs

Background: Because exposure to low temperature can modify the effect of vo latile anesthetics on airway smooth muscle contraction, this study was cond ucted to investigate low-temperature modifications of the inhibitory effect s of isoflurane and sevoflurane on canine tracheal smooth muscle tone by si multaneously measuring the muscle tension and intracellular concentration o f Ca2+ ([Ca2+](i)) and by measuring voltage-dependent Ca2+ channel activity . Methods: [Ca2+](i) was monitored by the 500-nm light emission ratio of prel oaded fura-2, a Ca2+ indicator. Isometric tension was measured simultaneous ly. Whole cell patch clamp recording techniques were used to observe voltag e-dependent Ca2+ channel activity in dispersed muscle cells. Isoflurane (0- 3.0%) or sevoflurane (0-3%) was introduced to a bath solution at various te mperatures (37, 34, or 31 degrees C). Results: Low temperature (34 or 31 degrees C) reduced high-K+-induced (72.7 mM) muscle contraction and increased [Ca2+](i), but it enhanced carbachol- induced (1 mu M) muscle contraction with a decrease in [Ca2+](i). The volat ile anesthetics tested showed significant inhibition of both high-K+-induce d and carbachol-induced airway smooth muscle contraction, with a concomitan t decrease in [Ca2+](i). The inhibition of the carbachol-induced muscle con traction by volatile anesthetics was abolished partially by exposure to low temperature. Volatile anesthetics and low-temperature exposure significant ly inhibited voltage-dependent Ca2+ channel activity of the smooth muscle. Conclusions: Exposure of airway smooth muscle to low temperature leads to a n increase in agonist-induced muscle contractility, with a decrease in [Ca2 +](i). The inhibition of voltage-dependent Ca2+ channel activity by exposur e to low temperature and by volatile anesthetics cam be attributed, at leas t in part, to the decrease in [Ca2+](i).