title: Analysis of the effects of fentanyl in the feline pulmonary vascular bed.
abstract: The objective of this study was to test the hypothesis that fentanyl induces a depressor response in the pulmonary vascular bed of the cat and to identify the receptors involved in the mediation or modulation of these effects. The authors conducted a prospective vehicle-controlled study at a university research laboratory using intact chest preparation in adult mongrel cats. In separate experiments, the effects of diphenhydramine (histamine receptor blocker), glibenclamide (ATP-sensitive K+ channel blocker), L-N5-(1-Iminoethyl) ornithine hydrochloride (L-NIO) (nitric oxide synthase inhibitor), nimesulide (selective cyclooxygenase [COX]-2 inhibitor), and naloxone (opiate receptor antagonist) were investigated on pulmonary arterial responses to fentanyl and other agonists in the pulmonary vascular bed of the cat. The systemic pressure and lobar arterial perfusion pressure were continuously monitored, electronically averaged, and recorded. In the feline pulmonary vascular bed of the isolated left lower lobe, fentanyl induced a dose-dependent vasodepressor response that was not significantly altered after administration of glibenclamide, L-NIO, and nimesulide. However, the responses to fentanyl were significantly attenuated after administration of diphenhydramine and naloxone. The results of the present study suggest that fentanyl has potent vasodepressor activity in the pulmonary vascular bed of the cat and that this response may be mediated or modulated by both histaminergic and opiate receptor sensitive pathways.
authors.affiliation: Department of Anesthesiology, LSU Health Sciences Center, New Orleans, Louisiana, USA. akaye@lsuhsc.edu
authors.forename: Alan D
authors.initials: AD
authors.lastname: Kaye
authors.forename: Jason M
authors.initials: JM
authors.lastname: Hoover
authors.forename: Ikhlass N
authors.initials: IN
authors.lastname: Ibrahim
authors.forename: James
authors.initials: J
authors.lastname: Phelps
authors.forename: Amir
authors.initials: A
authors.lastname: Baluch
authors.forename: Aaron
authors.initials: A
authors.lastname: Fields
authors.forename: Shane
authors.initials: S
authors.lastname: Huffman
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001920:Bradykinin / Q000378:metabolism; D002415:Cats; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004155:Diphenhydramine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005283:Fentanyl / Q000494:pharmacology*; D006632:Histamine / Q000378:metabolism; D006634:Histamine H1 Antagonists / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D011651:Pulmonary Artery / Q000187:drug effects* / Q000378:metabolism; D011652:Pulmonary Circulation / Q000187:drug effects; D011957:Receptors, Opioid / Q000187:drug effects* / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D000701:Analgesics, Opioid; D006634:Histamine H1 Antagonists; D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D014665:Vasodilator Agents; D009569:Nitric Oxide; D009270:Naloxone; D006632:Histamine; D004155:Diphenhydramine; D051546:Cyclooxygenase 2; D001920:Bradykinin; D005283:Fentanyl; D009638:Norepinephrine