期刊文献+

肝硬化大鼠Akt基因肝内转移对门静脉高压症血流动力学的影响

原文传递
导出
摘要 肝内血流阻力增加是门静脉高压症发病的始动原因,也是导致肝硬化患者发生并发症和死亡的主要原因。肝硬化时肝内血管阻力增加的一个重要原因是肝内血管的张力增加,这一因素受体内血管活性物质的调控。许多研究已经证实,肝硬化时肝窦内皮细胞受损,eNOS活性明显受抑,肝内NO生成减少是导致肝内血管阻力增加的重要原因,也与门静脉高压的形成和发展有密切关系,
出处 《中华外科杂志》 CAS CSCD 北大核心 2008年第22期1707-1709,共3页 Chinese Journal of Surgery
  • 相关文献

参考文献8

  • 1Bosch J, Garcia-Pagan JC. Complications of cirrhosis : Ⅰ. Portal hypertension. J Hepatol,2000,32 : 141-156.
  • 2邓刚,黄飞舟,刘浔阳,罗成群,郭立武.重组Akt腺病毒的构建及其在肝硬化大鼠肝脏中的表达[J].中国普通外科杂志,2008,17(7):687-691. 被引量:5
  • 3Garcia-Banuelos J,Siller-Lopez F, Miranda A, et al. Cirrhotic rat livers with extensive fibrosis can be safely transduced with clinicalgrade adenoviral vectors. Evidence of cirrhosis reversion. Gene Ther,2002,9 : 127-134.
  • 4Ludwig D,Schwarting K, Cornelia M, et al. The postprandial portal flow is related to the severity of portal hypertension and liver cirrhosis. Hepatology, 1998,28:631-638.
  • 5Gupta TK,Toruner M, Chung MK, et al. Endothelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats. Hepatology, 1998,28:926-931.
  • 6Rockey DC, Chung JJ. Reduced nitric oxide production by endothelial cells in cirrhotic rat liver: endothelial dysfunction in portal hypertension. Gastroenterology, 1998,114 : 344-351.
  • 7Uruno A, Sugawara A, Kanatsuka H, et al. Upregulation of nitric oxide production in vascular endothelial cells by all-trans retinoic acid through the phosphoinositide 3-kinase/Akt pathway. Circulation ,2005,112:727-736.
  • 8Sun Y, Sumi D, Kumagai Y. Serine 1179 phosphorylation of endothelial nitric oxide synthase caused by 2,4,6-trinitrotoluene through PI3K/Akt signaling in endothelial cells. Toxicol Appl Pharmacol, 2006,214 : 55 -60.

二级参考文献13

  • 1王旭东,刘虹,曹水,李慧,任秀宝,郝希山.表达转化生长因子βⅡ型受体胞外区-活化T细胞表达和分泌的调节因子融合基因重组腺病毒的构建与鉴定[J].中华实验外科杂志,2007,24(4):423-425. 被引量:1
  • 2孙敬方.动物实验方法学[M].北京:人民卫生出版社,2005:474-475.
  • 3Garcia-Banuelos J, Siller-Lopez F, Miranda A, et al. Cirrhotic rat livers with extensive fibrosis can be safely transduced with clinical-grade adenoviral vectors. Evidence of cirrhosis reversion[J]. Gene Ther,2002,9(2) : 127 -134.
  • 4Guicciardi ME, Gores GJ. Apoptosis : a mechanism of acute and chronic liver injury[ J] . Gut, 2005,54 ( 7 ) : 1024 - 1033.
  • 5Song E, Lee SK, Wang J, et al. RNA interference targeting Fas protects mice from fulminant hepatitis [ J ]. Nature Med, 2003,9(3) :347 -351.
  • 6Akazawa Y, Gores GJ. Death receptor-mediated liver injury [J]. Semin Liver Dis,2007,27(4) :327 -338.
  • 7Schattenberg JM, Galle PR, Schuchmann M. Apoptosis in liver disease [ J ] . Liver Int ,2006,26 ( 8 ) :904 - 911 .
  • 8Eichhorst ST. Modulation of apoptosis as a target for liver disease[J]. Expert Opin Ther Targets,2005,9 (1) :83 - 99.
  • 9Su CC, Lin YP, Cheng YJ, et al. Phosphatidylinositol 3- kinase/Akt activation by integrin-tumor matrix interaction suppresses Fas-mediated apoptosis in T cells [ J ]. J Immunol, 2007,179(7) :4589 -4597.
  • 10Franke TF, Homik CP, Segev L, et al. PI3 K/Akt and apoptosis: size matters [ J]. Oncogene, 2003, 22 (56) : 8983 -8998.

共引文献4

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