title: Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta.
abstract: In a previous study, we demonstrated that halothane and isoflurane inhibit binding of thromboxane A2 to its receptors on human platelets and thus inhibit prostanoid-induced aggregation strongly. The aim of this study was to determine whether volatile anaesthetics inhibit prostanoid-induced vasoconstriction preferentially. Rat isolated aortic rings were mounted in organ baths and their isometric tension was measured. They were contracted with STA2 (a stable thromboxane A2 analogue), prostaglandin F2 alpha (PGF2 alpha), phenylephrine, and 20 mM KCl, and then exposed to halothane (0.5-3%), isoflurane (0.5-3%), and sodium nitroprusside (SNP, 10(-9)-3 x 10(-7) M). Halothane (2-3%) and isoflurane (2-3%) induced greater relaxation of aortic rings precontracted with STA2 and PGF2 alpha than of those precontracted with phenylephrine (P < 0.01). Halothane induced greater relaxation of rings precontracted with KCl than phenylephrine only at 3%, whereas isoflurance relaxed rings precontracted with KCl more than those with phenylephrine at 0.5, 2 and 3% (P < 0.05). In contrast, SNP relaxed rings precontracted with PGF2 alpha. KCl and phenylephrine equally, but induced smaller relaxations of those precontracted with STA2 (P < 0.05). We conclude that halothane and isoflurane inhibit prostanoid-induced vasoconstriction preferentially, possibly by interacting with prostanoid receptors.
authors.affiliation: Department of Anesthesia, Kyoto University Hospital, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Hatano
authors.forename: M
authors.initials: M
authors.lastname: Kakuyama
authors.forename: H
authors.initials: H
authors.lastname: Hirakata
authors.forename: H
authors.initials: H
authors.lastname: Toda
authors.forename: N
authors.initials: N
authors.lastname: Seo
authors.forename: M
authors.initials: M
authors.lastname: Nishiwada
authors.forename: K
authors.initials: K
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Mori
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects*; D015237:Dinoprost / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006221:Halothane / Q000008:administration & dosage / Q000494:pharmacology*; D007530:Isoflurane / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D010208:Papaverine / Q000494:pharmacology; D010656:Phenylephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011982:Receptors, Prostaglandin / Q000187:drug effects; D017482:Receptors, Thromboxane / Q000187:drug effects; D013928:Thromboxane A2 / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D011982:Receptors, Prostaglandin; D017482:Receptors, Thromboxane; D009599:Nitroprusside; D010656:Phenylephrine; D013928:Thromboxane A2; D011189:Potassium Chloride; C037866:STA 2; D015237:Dinoprost; D007530:Isoflurane; D010208:Papaverine; D000109:Acetylcholine; D006221:Halothane