ABSTRACT
BACKGROUND: Volatile anesthetics are potent bronchodilators of airway smooth muscle. Bronchodilation is occured by depressing reflex neural pathways innervating airway smooth muscle and by acting directly on the smooth muscle cell. We studied the direct relaxation effect and their potency of halothane, isoflurane and desflurane on isolated rat distal bronchial segment of fourth order precontracted with acetylcholine. METHODS: Isolated Sprague-Dawley rat bronchial rings were suspended in tissue bath with modified- Krebs's solution. Based on the dose-response curve, the ED50 of acetylcholine (ACh) was calculated for fourth bronchial segment and administered to each tissue bath, after which the stabilized response was recorded. After then each bronchial segment with intact epithelium was exposed to increasing concentration of halothane, isoflurane and desflurane (1.0, 1.5 and 2.0 MAC)and the relaxant responses were recorded by polygraph. RESULTS: Halothane, isoflurane and desflurane produced concentration-dependent bronchodilation (P<0.05 for either anesthetics; 22 4%, 18 6%, 24 5% for halothane, isoflurane and desflurane at 1.5 MAC, 32 6%, 27 7%, 38 5% for halothane, isoflurane and desflurane at 2.0 MAC). Overall, desflurane had a significantly greater relaxing effect as compared with halothane, isoflurane at 1.5 MAC and 2.0 MAC during ACh-mediated contraction. CONCLUSION: The mechanism of halothane, isoflurane and desflurane-mediated bronchodilation is not known, but may be due to an epithelium dependent effect. The potency of relaxing the ACh precontracted isolated rat bronchial smooth muscle is desflurane, halothane, isoflurane in ordered.
Subject(s)
Animals , Rats , Acetylcholine , Anesthetics , Baths , Bronchi , Bronchodilator Agents , Epithelium , Halothane , Isoflurane , Muscle, Smooth , Myocytes, Smooth Muscle , Neural Pathways , Rats, Sprague-Dawley , Reflex , RelaxationABSTRACT
BACKGROUND: Volatile anesthetics are potent bronchodilators of airway smooth muscle. Bronchodilation is occured by depressing reflex neural pathways innervating airway smooth muscle and by acting directly on the smooth muscle cell. We studied the direct relaxation effect and their potency of halothane, isoflurane and desflurane on isolated rat distal bronchial segment of fourth order precontracted with acetylcholine. METHODS: Isolated Sprague-Dawley rat bronchial rings were suspended in tissue bath with modified- Krebs's solution. Based on the dose-response curve, the ED50 of acetylcholine (ACh) was calculated for fourth bronchial segment and administered to each tissue bath, after which the stabilized response was recorded. After then each bronchial segment with intact epithelium was exposed to increasing concentration of halothane, isoflurane and desflurane (1.0, 1.5 and 2.0 MAC)and the relaxant responses were recorded by polygraph. RESULTS: Halothane, isoflurane and desflurane produced concentration-dependent bronchodilation (P<0.05 for either anesthetics; 22 4%, 18 6%, 24 5% for halothane, isoflurane and desflurane at 1.5 MAC, 32 6%, 27 7%, 38 5% for halothane, isoflurane and desflurane at 2.0 MAC). Overall, desflurane had a significantly greater relaxing effect as compared with halothane, isoflurane at 1.5 MAC and 2.0 MAC during ACh-mediated contraction. CONCLUSION: The mechanism of halothane, isoflurane and desflurane-mediated bronchodilation is not known, but may be due to an epithelium dependent effect. The potency of relaxing the ACh precontracted isolated rat bronchial smooth muscle is desflurane, halothane, isoflurane in ordered.
Subject(s)
Animals , Rats , Acetylcholine , Anesthetics , Baths , Bronchi , Bronchodilator Agents , Epithelium , Halothane , Isoflurane , Muscle, Smooth , Myocytes, Smooth Muscle , Neural Pathways , Rats, Sprague-Dawley , Reflex , RelaxationABSTRACT
BACKGROUND: Lidocaine is often administered intravenously to suppress airway reflexes associated with tracheal intubation or tracheal suction. In addition, lidocaine is known to have airway relaxant effects through a direct relaxant mechanism on the smooth muscle. The presence of airway epithelium has been reported to reduce the sensitivity and maximum contractile response to histamine or acetylcholine(ACh). The purpose of this study was to determine whether the cumulative application of lidocaine may cause a concentration-dependent relaxation of the rat tracheal smooth muscle strips with intact or rubbed epithelium. METHODS: Using the rat tracheal smooth muscle strips, the effects of 10 6~3 10 3M of lidocaine pretreatment on isometric tension induced by 40 mM of K+ or 10 5M of ACh in presence or absence of adherent epithelium, and the influences of 10 6M of propranolol, 10 4M of L-NAME and 10 6M of atropine on relaxing response of lidocaine were studied. RESULTS: The tracheal smooth muscle concentration induced by K+ and ACh was similar magnitude both in presence or absence of adherent epithelium. The removal of epithelium did not affect the relaxant effect of lidocaine on the K+ and ACh-induced tracheal smooth muscle contraction. Lidocaine pretreatment reduced Ca2+-dependent contraction of the rat tracheal smooth muscle. Following pretreatment of the tracheal smooth muscle preparations respectively with propranolol, L-NAME and atropine the relaxing responses to lidocaine of tracheal smooth muscle were not depressed. CONCLUSIONS: These results suggest that the effect of the epithelium on lidocaine-induced relaxation of the tracheal smooth muscle is not significant and lidocaine may directly relax tracheal smooth muscle by the influences on the Ca2+ mobilization.