title: Factors influencing the direct actions of volatile anesthetics on airway smooth muscle.
abstract: BACKGROUND
  The authors hypothesized that the ability of volatile anesthetics to relax airway smooth muscle (AWSM) depends on: 1) the agonist used to produce muscle contraction, 2) the preexisting level of contraction, and 3) the volatile anesthetic used.
  
  
  METHODS
  To test the first hypothesis, isolated strips of canine trachealis muscle were precontracted with acetylcholine (ACh), McN-A-343 (McN, another muscarinic agonist), 5-hydroxytryptamine (5HT, a different receptor agonist), or potassium chloride (KCl, which induces contraction by cell depolarization) to 50% of maximal force, then exposed to halothane (0.2-1.6 MAC). To test the second and third hypotheses, other strips were precontracted to 25, 50, 75, and 100% of maximal force with ACh, or to 10, 30, or 50% of maximal force with KCl, and were then exposed to halothane or isoflurane (0.2-1.6 MAC).
  
  
  RESULTS
  For AWSM contracted to 50% of maximal force, the amount of relaxation produced by halothane depended on the agonist used to elicit contraction in the following manner: 5HT = McN > ACh; the muscles contracted with KCL did not relax. For ACh-induced contractions, the absolute amount of relaxation produced by halothane did not depend on the level of precontraction. In muscles contracted with KCl, the volatile anesthetics caused significant relaxation only in muscles contracted to 10% of maximal force. Overall, halothane had a significantly greater relaxing effect as compared with isoflurane during ACh-mediated contractions; the effects of the two agents did not differ significantly during KCl-mediated contractions.
  
  
  CONCLUSIONS
  When canine AWSM tone is increased by contractile agonists in vitro, the absolute amount of relaxation produced by halothane depends on the agonist used to elicit contraction, but not the degree of precontraction. In addition, there are small but significant differences between the effects of halothane and isoflurane on ACh-mediated contractions.
authors.affiliation: Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55906.
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: N
authors.initials: N
authors.lastname: Morimoto
authors.forename: D O
authors.initials: DO
authors.lastname: Warner
authors.forename: K
authors.initials: K
authors.lastname: Rehder
authors.forename: K A
authors.initials: KA
authors.lastname: Jones
mesh_terms: D008455:(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride / Q000037:antagonists & inhibitors; D000109:Acetylcholine / Q000037:antagonists & inhibitors; D000818:Animals; D004285:Dogs; D006221:Halothane / Q000494:pharmacology*; D066298:In Vitro Techniques; D007530:Isoflurane / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects* / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D011189:Potassium Chloride / Q000037:antagonists & inhibitors; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology; D014132:Trachea
chemical_list: D008455:(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride; D000109:Acetylcholine; D006221:Halothane; D007530:Isoflurane; D011189:Potassium Chloride; D017367:Selective Serotonin Reuptake Inhibitors