期刊文献+

术后败血症患者肝功能损害与一氧化氮产生的关系 被引量:1

Relationship between nitric oxide production and hepatic dysfunction in patients with postoperative sepsis
原文传递
导出
摘要 目的探讨手术后败血症患者肝功能损害与一氧化氮产生的关系。方法将20例接受腹部手术并在术后发生败血症的患者分成两组:存活组、死亡组。在发生败血症之前取血样,并在发生败血症后每隔3d取1次血样,直到患者死亡或出院。分析稳定的NO基团代谢终产物(NOx)和动脉内KBR(AKBR)的关系。结果术后发生败血症的患者中,7例死亡患者的血浆NOx水平比13例存活患者显著增高。死亡组患者的AKBR水平比存活组显著降低,这表明死亡组患者的肝功能受到损害。与之比较,死亡组血浆NOX水平比存活组显著增高。当AKBR的水平降到0.7以下时,NOX的水平开始升高。此外,血浆AKBR水平的变化程度受NOX水平的影响,这表明NO与肝脏细胞的线粒体功能障碍有一定关系。结论NO的过量产生可能是导致术后败血症患者出现致命性代谢功能紊乱的原因之一。 Objective To discuss the relationship between nitric oxide (NO) production and hepatic dysfunction in patients with postoperative sepsis. Methods Twenty patients with sepsis following abdominal abdominal surgery were divided into two groups: survival group and dead group. Blood samples were collected before and every 3 days after the development of postoperative sepsis. The relationship between stable metabolic end product of NO group (NOx) and the arterial KBR (AKBR) was analyzed. Resuits Plasma NOx levels in 7 dead patients with postoperative sepsis were higher than in survival group. In dead group, the AKBR was significantly lower than in survival group, indicating the impaired hepatic function. In contrast, plasma NOx levels in dead group were significantly higher than in survival group. When the level of AKBR was decreased to below 0.7 in dead group, NOx levels began to increase. Moreover, plasma NOx levels were closely correlated with the AKBR, indicating that NO group was associated with mitochondrial dysfunction in the liver. Conclusion It is likely that the overproduction of NO group plays an important role in causing fatal metabolic disorders in patients with postoperative sepsis.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2008年第4期507-509,共3页 Chinese Journal of Experimental Surgery
关键词 一氧化氮 肝功能衰竭 酮体 Nitric oxide Hepatic failure Ketone body
  • 相关文献

参考文献8

  • 1Eum HA,Park SW, Lee SM, et al. Role of nitric oxide in the expression of hepatic vascular stress genes in response to sepsis. Nitric oxide,2007,17:126-133.
  • 2Luiking YC,Deutz NE. Exogenous arginine in sepsis. Crit Care Med, 2007,35:557-563.
  • 3Philippart F, Cavaillon JM. Sepsis mediators. Curt Infect Dis Rep, 2007,9:358-365.
  • 4Cui X, Besch V, KhaibuUina A, et al. Neuronal nitric oxide synthase deficiency decreases survival in bacterial peritonitis and sepsis. Intensive Care Med,2007,33:1993-2003.
  • 5Cauwels A. Nitric oxide in shock. Kidney Int ,2007,72:557-565.
  • 6Cui X. Members of the american college of chest physicians/society of critical care medicine consensus conference committee. American college of chest physicians/society of critical care medicine consensus conference:definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med ,1992,20:864- 874.
  • 7Uno S,Hoh M,Kurono Y,et al. A simple and sensitive assay for blood ketone bodies using highly purified 3-hydroxybutyrate dehydrogenase. Clin. Chim. Acta, 1987,168:253-255.
  • 8Knaus WA,Draper EA,Wagner DP,et al. APACHE:A severity of disease classitication system. Crit Care Med,1985 ,13 :818.-829.

同被引文献5

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部