title: Halothane anesthesia causes active flow-independent pulmonary vasoconstriction.
abstract: We utilized multipoint pulmonary vascular pressure-flow (P/Q) plots to investigate the effects of halothane anesthesia on the pulmonary circulation. Our first objective was to assess the extent to which the P/Q relationship measured in conscious dogs is altered during halothane anesthesia. P/Q plots were constructed by stepwise constriction of the thoracic inferior vena cava to decrease venous return and Q. Compared with conscious dogs, halothane (approximately 1.2% end-tidal) resulted in active, flow-independent pulmonary vasoconstriction (P less than 0.01) at all levels of Q. Halothane also decreased (P less than 0.01) systemic arterial pressure and Q. Thus our second objective was to determine whether the halothane-induced pulmonary vasoconstriction was mediated by reflex neurohumoral activation or by metabolites of the cyclooxygenase pathway. However, the magnitude of halothane-induced pulmonary vasoconstriction was not significantly reduced by sympathetic alpha-adrenoreceptor block, angiotensin converting-enzyme inhibition, combined arginine vasopressin V1 + V2 receptor block, or by cyclooxygenase inhibition. Finally, halothane-induced pulmonary vasoconstriction (P less than 0.01) was also observed when compared with pentobarbital-anesthetized dogs during controlled ventilation. Thus, compared with the conscious state, halothane anesthesia causes active flow-independent pulmonary vasoconstriction that is not mediated by reflex neurohumoral activation, by metabolites of the cyclooxygenase pathway, nor is it due to the effects of general anesthesia and controlled ventilation.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
authors.forename: B B
authors.initials: BB
authors.lastname: Chen
authors.forename: D P
authors.initials: DP
authors.lastname: Nyhan
authors.forename: D M
authors.initials: DM
authors.lastname: Fehr
authors.forename: H M
authors.initials: HM
authors.lastname: Goll
authors.forename: P A
authors.initials: PA
authors.lastname: Murray
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000769:Anesthesia, Inhalation; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001784:Blood Gas Analysis; D016861:Cyclooxygenase Inhibitors; D004285:Dogs; D006221:Halothane / Q000008:administration & dosage / Q000494:pharmacology*; D006439:Hemodynamics / Q000502:physiology; D008168:Lung / Q000098:blood supply; D010424:Pentobarbital / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D011652:Pulmonary Circulation / Q000187:drug effects / Q000502:physiology; D011667:Pulmonary Veins / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D011945:Receptors, Angiotensin / Q000187:drug effects; D017483:Receptors, Vasopressin; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology; D014692:Ventilation-Perfusion Ratio / Q000187:drug effects / Q000502:physiology
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D016861:Cyclooxygenase Inhibitors; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D010424:Pentobarbital; D006221:Halothane