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Analysis of the metabolic disorder based on the redox theory in the septic patient induced by nitric oxide

Analysis of the metabolic disorder based on the redox theory in the septic patient induced by nitric oxide
基于氧化还原理论的一氧化氮所致脓毒症患者代谢紊乱分析
批准号:
10671227
负责人:
KANEMAKI Toshiki
金额:
$0.32万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999

项目摘要

项目成果

相关文献

中文摘要
翻译
硝酸氧化物(NO)在初级文化大鼠中生产,使用无监测器观察2小时。这些发现与灰色代理法相同,也是用硝酸盐来衡量的。However,两小时后,我们将无法检测到NO.对没有监测器影响测量的葡萄糖的附着物。硝酸氧化物的生产及其对能量代谢的影响被调查到从肝脏残留物后获得的文化大鼠葡萄糖。hepatocytes obtained from liver remnant after partial hepatectomy (HPH) produced more nitric oxide than hepatocytes obtained from sham operated liver (HS), following stimulation with IL-1\。在我们最近的研究中,IL-1 β显示了刺激硝酸氧化物(NO)在培养大鼠的谷胱甘肽中产生,并降低了酮体比率(KBR :乙酸酯/b-羟基丁酸酯)。The reduced KBR, reflecting the liver mitochon?al redox state (NAD D1+イエD1/NADH), resulted in the inhibition of ATP synthesis。在目前的研究中, KBR在文化HPH中的含量低于HS。晚期,腺苷核肽含量(ATP, ADP和AMP)低于HS中的HPH。这些结果提出了以下结论:在感染期间,肝脏是一个更容易被怀疑的线粒体动力失调作为硝酸氧化物产生的一个结果。类似的结果是,在从obstructive jaudice rat中观察到的Hepatocytes,在融合中,在部分hepatectomy demonstrated increased NO生产后,在局部hepatectomy demonstrated increased in NO生产中表现为增加敏感性到IL-1 βNO,原因是liver dysfunction后由于hepatectomy因为没有诱导性hepatochondria dysfunction。
英文摘要
Nitric oxide (NO) production in primary cultured rat hepatocytes were observed for 2 hours using the NO monitor. These findings were the same as nitrite measured by Griess reagent method. However, after 2 hours, we would not detected the NO. The attachment of the hepatocytes to the NO monitor affected the measurement.Nitric oxide production and its effect on energy metabolism was investigated in cultured rat hepatocytes obtained from the liver remnant after partial hepatectomy. The hepatocytes obtained from liver remnant after partial hepatectomy (HPH) produced more nitric oxide than hepatocytes obtained from sham operated liver (HS), following stimulation with IL-1β. In our recent study, IL-1β was shown to stimulate nitric oxide (NO) production in cultured rat hepatocytes and NO reduced the ketone body ratio (KBR : acetoacetate/b-hydroxybutyrate). The reduced KBR, reflecting the liver mitochondrial redox state (NADィイD1+ィエD1/NADH), resulted in the inhibition of ATP synthesis. In the present study, KBR in the medium of cultured HPH was lower than that of HS. Furthermore, adenine nucleotides content (ATP, ADP and AMP) was lower in HPH than in HS. These results suggest that following partial hepatectomy, the liver is more susceptible to mitochondrial dysfunction as a result of the nitric oxide produced during infection. The similar results ware observed in hepatocytes obtained from obstructive jaudice rat.In conclusion, hepatocytes in the liver remnant after partial hepatectomy demonstrated increased NO production which was attributed to increased sensitivity to IL-1βNO in turn, cause liver dysfunction after hepatectomy because NO induces hepatic mitochondria dysfunction.
期刊论文(2)
专著(0)
科研奖励(0)
会议论文
Tu Wei: "An Enhancement of Nitric Oxide Production Regulates Energy Metabolism in Rat Hepatocytes after a Partial Hepatectomy"Journal of Hepatology. 30. 944-950 (1999)
涂伟:“一氧化氮生成的增强调节部分肝切除术后大鼠肝细胞的能量代谢”肝脏病学杂志。
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通讯作者:
Satoi S, Kamimaya Y, Kitade H, Kwon A-H, Takahashi K, Tu Wei, Inoue T, Takahashi H: "Nitric Oxide Production and Hepatic Dysfunction in Patients with Postoperative Sepsis."Clinical and Experimental Pharmacology and Physiology. (in press). (2000)
Satoi S、Kamimaya Y、Kitade H、Kwon A-H、Takahashi K、Tu Wei、Inoue T、Takahashi H:“术后脓毒症患者的一氧化氮产生和肝功能障碍。”临床和实验药理学和生理学。
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