title: Combined neurohumoral block modulates pulmonary vascular P/Q relationship in conscious dogs.
abstract: Our objective was to investigate the integrated pulmonary vascular response of conscious dogs to combined inhibition of the autonomic nervous system, arginine vasopressin (V1) receptors (vasopressinergic V1), and converting enzyme to identify the overall influence of these three major neurohumoral mechanisms in vascular regulation of the pulmonary circulation. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were generated by graded constriction of the thoracic inferior vena cava, which produced stepwise decreases in Q. When compared with the P/Q relationship measured in intact conscious dogs, combined neurohumoral block resulted in active, nonflow-dependent pulmonary vasodilation. A second objective was to assess the extent to which cyclooxygenase pathway inhibition modified both the intact P/Q relationship and the pulmonary vasodilator response to combined neurohumoral block. Cyclooxygenase inhibition alone (either indomethacin or sodium meclofenamate) resulted in active, nonflow-dependent pulmonary vasoconstriction. Moreover, the pulmonary vasodilation in response to combined neurohumoral block was entirely abolished following cyclooxygenase inhibition. Thus the integrated pulmonary vascular response of conscious dogs to combined neurohumoral block is active vasodilation. This response appears to be mediated by metabolites of the cyclooxygenase pathway.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
authors.forename: H S
authors.initials: HS
authors.lastname: Geller
authors.forename: D P
authors.initials: DP
authors.lastname: Nyhan
authors.forename: H M
authors.initials: HM
authors.lastname: Goll
authors.forename: P W
authors.initials: PW
authors.lastname: Clougherty
authors.forename: B B
authors.initials: BB
authors.lastname: Chen
authors.forename: P A
authors.initials: PA
authors.lastname: Murray
mesh_terms: D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000502:physiology*; D001794:Blood Pressure; D001835:Body Weight; D002216:Captopril / Q000494:pharmacology; D002302:Cardiac Output; D016861:Cyclooxygenase Inhibitors; D004285:Dogs; D006439:Hemodynamics; D007213:Indomethacin / Q000494:pharmacology; D008168:Lung / Q000098:blood supply*; D008469:Meclofenamic Acid / Q000494:pharmacology; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000187:drug effects / Q000502:physiology*; D017483:Receptors, Vasopressin; D014664:Vasodilation / Q000187:drug effects
chemical_list: D016861:Cyclooxygenase Inhibitors; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D008469:Meclofenamic Acid; D001285:Atropine; D002216:Captopril; D011433:Propranolol; D007703:Peptidyl-Dipeptidase A; D011224:Prazosin; D007213:Indomethacin