title: Interaction between halothane and the nonadrenergic, noncholinergic inhibitory system in porcine trachealis muscle.
abstract: BACKGROUND
  Volatile anesthetics significantly affect cholinergic neural transmission in the airways and relax airway smooth muscle. Activation of the nonadrenergic, noncholinergic inhibitory neural pathway, which is thought to be mediated by nitric oxide, relaxes human and procine airways. The purpose of the current study was to determine in the isolated porcine trachealis muscle whether relaxation of airway smooth muscle by halothane is mediated in part by activation of the nonadrenergic, noncholinergic inhibitory system.
  
  
  METHODS
  Isometric tension was measured in porcine trachealis muscle suspended in tissue baths in the presence of propranalol (10(-6) M). After stimulation of postsynaptic nicotinic cholinergic receptors with 1,1-dimethyl-4-phenyl-piper-azinium iodide (10(-4) M) to prevent contractile responses to subsequent electrical field stimulation, carbachol (3 x 10(-7) M) was added to increase tone. Nonadrenergic, noncholinergic relaxation responses to electrical field stimulation were then measured in the presence of inhibitors of nitric oxide synthase or L-arginine (the substrate for nitric oxide synthase), in the presence and absence halothane.
  
  
  RESULTS
  Electrical field stimulation produced frequency-dependent relaxations that were attenuated by inhibitors of nitric oxide synthase (NG-nitro-L-arginine methyl ester [L-NAME] or NG-monomethyl-L-arginine, 10(-4) M). Pretreatment with L-arginine (10(-4) M) prevented the effect of L-NAME. Halothane (0.5% or 1.0%) neither enhanced nor attenuated nonadrenergic, noncholinergic relaxations in the presence of L-NAME, D-NAME, L-arginine, or D-arginine.
  
  
  CONCLUSIONS
  Halothane, at concentrations < or = 1.0%, does not relax porcine airway smooth muscle in vitro by activating the nonadrenergic, noncholinergic inhibitory system.
authors.affiliation: Department of Environmental Health Sciences, Johns Hopkins Hospital School of Hygiene and Public Health, Baltimore, Maryland 21205.
authors.forename: K S
authors.initials: KS
authors.lastname: Lindeman
authors.forename: S G
authors.initials: SG
authors.lastname: Baker
authors.forename: C A
authors.initials: CA
authors.lastname: Hirshman
mesh_terms: D018674:Adrenergic Antagonists; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D018680:Cholinergic Antagonists; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology; D006221:Halothane / Q000494:pharmacology*; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester; D009434:Neural Pathways / Q000187:drug effects; D009569:Nitric Oxide / Q000502:physiology; D011941:Receptors, Adrenergic / Q000187:drug effects*; D011950:Receptors, Cholinergic / Q000187:drug effects*; D013552:Swine; D009435:Synaptic Transmission / Q000187:drug effects; D014132:Trachea / Q000187:drug effects* / Q000502:physiology
chemical_list: D018674:Adrenergic Antagonists; D018680:Cholinergic Antagonists; D011941:Receptors, Adrenergic; D011950:Receptors, Cholinergic; D009569:Nitric Oxide; D004246:Dimethylphenylpiperazinium Iodide; D002217:Carbachol; D001120:Arginine; D006221:Halothane; D019331:NG-Nitroarginine Methyl Ester