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1 Department of Physiology, Division 2, Kanazawa Medical University, Uchinada, Ishikawa, Japan; First Department of Medicine, Shinshu Universtiy School of Medicine, Matsumoto, Nagano, Japan
2 Department of Physiology, Division 2, Kanazawa Medical University, Uchinada, Ishikawa, Japan
3 Department of Physiology, Division 2, Kanazawa Medical University, Uchinada, Ishikawa, Japan; Department of Anesthesiology, Kanazawa Medical University, Uchinada, Ishikawa, Japan
4 Department of Anesthesiology, Kanazawa Medical University, Uchinada, Ishikawa, Japan
5 First Department of Medicine, Shinshu Universtiy School of Medicine, Matsumoto, Nagano, Japan
6 Department of Pharmacology, Kanazawa Medical University, Uchinada, Ishikawa, Japan
* To whom correspondence should be addressed. E-mail: shibamo{at}kanazawa-med.ac.jp.
The pathophysiology of 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. Using 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.
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