Role of nitric oxide in oxygen transport in rat liver sinusoids during endotoxemia

Role of nitric oxide in oxygen transport in rat liver sinusoids during endotoxemia
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DOI:
10.1002/hep.510260213
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发表时间:
1997-08-01
期刊:
影响因子:
13.5
通讯作者:
Matsuda, H
Matsuda, H
中科院分区:
医学1区
文献类型:
--
作者:
Huang, TP;Nishida, T;Matsuda, H

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为了探讨一氧化氮(NO)在内毒素血症时肝微循环和肝损伤中的作用,我们研究了内毒素融合大鼠肝微循环中O-2的转运。大鼠连续灌胃大肠杆菌脂多糖(LPS) (0.8 mg/kg/h) 7小时。LPS升高血浆NO2- + NO3-和天冬氨酸转氨酶(AST)水平,降低胆汁行率和肝三磷酸腺苷(ATP)水平。通过两种方法评估肝脏微循环:反射分光光度法显示肝脏中血红蛋白(Hb)的氧合减少,双点微光谱法显示LPS处理降低了血流速度、Hb的氧合和从窦状体到肝细胞的Oz释放。观察到的Oz输运参数的降低在中心周围、正弦波中表现突出。n -w-硝基- l -精氨酸甲酯(L-NAME) (5 mg/kg/h)和氨基胍(AMG) (5 mg/kg/h)加LPS可进一步加重这些现象,同时给予l -精氨酸(L-Arg) (100 mg/kg/h)可逆转这些现象。提示NO可改善内毒素引起的肝氧转运和肝功能恶化。
To evaluate the role of nitric oxide (NO) in hepatic microcirculation and liver injury during endotoxemia, we studied O-2 transport in the hepatic microcirculation of endotoxin-fused rats. Rats were continuously infused with Escherichia coli lipopolysaccharide (LPS) (0.8 mg/kg/h) for 7 hours. LPS increased the plasma levels of NO2- + NO3- and aspartate transaminase (AST), and decreased the bile Row rate and hepatic adenosine triphosphate (ATP) level. Hepatic microcirculation was evaluated by two methods: reflectance spectrophotometry showed a decrease in the oxygenation of hemoglobin (Hb) in the liver, and dual-spot microspectroscopy indicated that LPS administration decreased blood velocity, the oxygenation of Hb, and Oz release from sinusoids to hepatocytes. The observed decreases in the Oz transport parameters were prominent in pericentral, sinusoids. AU of these phenomena were further aggravated by the administration of N-w-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg/h) plus LPS, and by aminoguanidine (AMG) (5 mg/kg/h) plus LPS, and these could be reversed by the concomitant administration of L-arginine (L-Arg) (100 mg/kg/h). These results suggest that deterioration of hepatic oxygen transport and liver function induced by endotoxin can be ameliorated by NO.