摘要
肝硬化普遍存在着高动力循环状态，一些血管扩张物质参与了这种异常状态的发生。为探讨扩血管物质一氧化氮在肝硬化时的水平及其产生机制，测定了３８例肝硬化患者及１５例正常对照者血浆中一氧化氮代谢产物ＮＯ２－／ＮＯ３－及内毒素、肿瘤坏死因子α（ＴＮＦα）、环磷酸鸟苷（ｃＧＭＰ）含量。结果发现，ＮＯ２－／ＮＯ３－水平较正常对照显著升高，与增多的内毒素、ＴＮＦα水平呈正相关，血中ＮＯ２－／ＮＯ３－水平随肝功能Ｃｈｉｌｄ－Ｐｕｇｈ分级增加而升高。提示肝硬化时，一氧化氮合成增加，且与内毒素、ＴＮＦα诱导有关，前者可能是肝硬化血液动力学紊乱等产生的重要原因。
The aim of this study is to ascertain whether the formation of nitric oxide is argumented in patients with liver cirrhosis and its mechanism. 38 cirrhotic patients and 15 normal controls were studied. Higher plasma levels of NO 2 -/NO 3 - (stable end products of nitric oxide), endotoxin, tumor necrosis factor α (TNFα) and cyclic guanosine monophosphate (cGMP) were observed in patients with cirrhosis than in normal controls ( P <0.01, 0.01, 0.01, 0.05). The higher Child Pugh, the higher plasma NO 2 -/NO 3 - level. The concentration of NO 2 -/NO 3 - had a positive correlation with that of endotoxin and TNFα ( r = 0.481 , P <0.01; r =0.351, P <0.05). It is suggested that the production of nitric oxide is augmented and could be induced by endotoxin and TNFα. Execessive formation of nitric oxide may be related to hyperdynamic circulation in cirrhosis.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1997年第1期25-27,共3页
Chinese Journal of Internal Medicine
基金
湖北省科委基金
关键词
肝硬化
一氧化氮
内毒素类
肿瘤坏死因子
Liver cirrhosis Nitric oxide Endotoxins Tumor necrosis factor
