Role of nitric oxide in the expression of hepatic vascular stress genes in response to sepsis
- Authors
- Eum, HA[Eum, Hyun-Ae]; Park, SW[Park, Sang-Won]; Lee, SM[Lee, Sun-Mee]
- Issue Date
- Nov-2007
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- cecal ligation and puncture; liver dysfunction; microcirculation; nitric oxide; vasoregulatory gene expression
- Citation
- NITRIC OXIDE-BIOLOGY AND CHEMISTRY, v.17, no.3-4, pp.126 - 133
- Indexed
- SCIE
SCOPUS
- Journal Title
- NITRIC OXIDE-BIOLOGY AND CHEMISTRY
- Volume
- 17
- Number
- 3-4
- Start Page
- 126
- End Page
- 133
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/83619
- DOI
- 10.1016/j.niox.2007.08.003
- ISSN
- 1089-8603
- Abstract
- This study examined the role of nitric oxide (NO) on the expression of the hepatic vasoregulatory gene during polymicrobial sepsis. Aminoguanidine (AG, 100 mg/kg) or N-omega-nitro-L-arginine methyl ester (L-NAME, 100 mg/kg) was injected intraperitoneally at 0, 3, 6, 10, and 20 h after a cecal ligation and puncture (CLP). The heart rate increased 24 It after the CLP, and this increase was attenuated by L-NAME and further attenuated by AG. The mean arterial pressure in the CLP animals did not change significantly 24 h after the onset of sepsis but was increased after the L-NAME injection. Sepsis increased the serum aminotransferase levels, which were attenuated by AG but augmented by L-NAME. CLP increased the mRNA level of the ET-1 and ETB receptors in the liver. This increase was prevented by AG but augmented by L-NAME. The level of iNOS and HO-1 mRNA expression were increased by CLP, which was prevented by both AG and L-NAME. The level of TNF-alpha and COX-2 mRNA expression increased after CLP, and was attenuated by AG. These results show that iNOS and eNOS are regulated differently in sepsis. While eNOS appears to have a protective role in liver microcirculation, the strong upregulation of NOS might contribute to a microvascular dysfunction and hepatic injury. (c) 2007 Elsevier Inc. All rights reserved.
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Collections - Pharmacy > Department of Pharmacy > 1. Journal Articles
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