title: NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver.
abstract: The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (Pdo), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in Rpv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor NG-nitro-l-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both Rpv and Rhv (2.2- and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre- and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses.
authors.affiliation: Department of Physiology, Division 2, Kanazawa Medical University, Uchinada 920-0293, Japan.
authors.forename: Zonghai
authors.initials: Z
authors.lastname: Ruan
authors.forename: Toshishige
authors.initials: T
authors.lastname: Shibamoto
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Shimo
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tsuchida
authors.forename: Tomonobu
authors.initials: T
authors.lastname: Koizumi
authors.forename: Matomo
authors.initials: M
authors.lastname: Nishio
mesh_terms: D000707:Anaphylaxis / Q000209:etiology / Q000503:physiopathology*; D000818:Animals; D001646:Bile / Q000378:metabolism; D002248:Carbon Monoxide / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006168:Guinea Pigs; D006439:Hemodynamics / Q000187:drug effects; D006503:Hepatic Veins / Q000503:physiopathology; D007114:Immunization; D066298:In Vitro Techniques; D007267:Injections; D008099:Liver / Q000187:drug effects* / Q000503:physiopathology*; D008102:Liver Circulation / Q000187:drug effects; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000494:pharmacology*; D009929:Organ Size; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D011169:Portal Vein / Q000503:physiopathology; D011524:Protoporphyrins / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D015430:Weight Gain
chemical_list: D004791:Enzyme Inhibitors; D011524:Protoporphyrins; C017803:zinc protoporphyrin; D009569:Nitric Oxide; D002248:Carbon Monoxide; D010047:Ovalbumin; D019331:NG-Nitroarginine Methyl Ester