Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/68435
標題: Obstructive Jaundice Activates Nitroxidergic Neurons of the Vago-Vagal Neural Circuit That Regulates the Hepatobiliary System in Rabbits
作者: Hu, M.E.
Lin, Y.C.
Chang, H.M.
Tyan, Y.S.
Lan, C.T.
關鍵字: Bile duct ligation;Nitric oxide synthase;Nicotinamide adenine;dinucleotide phosphate-diaphorase;Nodose ganglion;Nucleus of solitary;tract;Dorsal motor vagal nucleus;nitric-oxide synthase;extrahepatic biliary system;isolated rat;hepatocytes;dorsal motor nucleus;canalicular contraction;portal-hypertension;endothelial-cells;afferent activity;hepatic-fibrosis;neuropeptide-y
Project: Cells Tissues Organs
期刊/報告no:: Cells Tissues Organs, Volume 195, Issue 3, Page(s) 272-286.
摘要: 
In this study, we investigated the expression of neuronal nitric oxide synthase (nNOS) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), two specific enzymes for nitric oxide (NO) synthesis, in the development of liver fibrosis induced by chronic bile duct ligation (BDL) in the rabbit. We specifically studied the liver-innervated nitroxidergic neurons that originate in the nodose ganglion (NG), nucleus of the solitary tract (NTS) and dorsal motor vagal nucleus (DMV). Our data showed that BDL resulted in overexpression of NADPH-d/nNOS in the NG, NTS and DMV neurons. Using densitometric analysis, we found a significant increase in NADPH-d expression as a result of BDL in the NG, NTS and DMV (72.6, 79.4 and 57.4% increase, respectively). These findings were corroborated by serum biochemistry and hepatic histopathological examination, which were influenced by NADPH-d/nNOS-generated NO in the liver following BDL. Upregulation of NADPH-d/nNOS expression may have important implications, including (1) facilitation of extrahepatic biliary parasympathetic tone that promotes gallbladder emptying of excess stagnant bile; (2) relaxation of smooth muscles of bile canaliculi thus participating in the pathogenesis of cholestasis; (3) dilation of hepatic sinusoids to counter BDL-induced intrahepatic portal hypertension in which endothelia may be damaged, and (4) alterations in hepatic metabolism, such as glycogenesis, bile formation and secretion, and bilirubin clearance. Copyright (C) 2011 S. Karger AG, Basel
URI: http://hdl.handle.net/11455/68435
ISSN: 1422-6405
DOI: 10.1159/000324929
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