الفهرس 
Role of angiotensin II (Ang II) in tracheal reactivity of rats exposed to ischemia reperfusion injury of liver
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Abstract
Back ground: Lung injury is one of the most popular consequences of hepatic ischemia /reperfusion (I/R) injury. Recently it was documented that renin angiotensin system (RAS) play a key role in tissue inflammation, and generated reactive oxygen specious (ROS) during I/R are the principal mediators of liver injury. Local tissue hypoxia and impaired production of adenosine triphosphate (ATP) production all could enhance production of ROS, proinflammatory cytokines, vasoactive agents, and increased expression of adhesion molecules. Objective: The purpose of this study is to determine the role of angiotensin II in tissue inflammation and the protective effect of acute and chronic administration of angiotensin converting enzyme (ACE) inhibitor (captopril) on hepatic inflammation and lung injury caused by hepatic ischemia induced for 1 hour followed by 24 hours of reperfusion. Methods: forty male rats were divided into 4 groups: group I: Sham operated group, group II: experimental model of hepatic I/R, group III: I/R with acute captopril administration at dose 100 mg/ kg body weight 24 and 1.5 hour before ischemia reperfusion injury and group IV: I/R with chronic captopril administration at dose 10 mg/kg body weight daily for 28 days before ischemia reperfusion injury. At the end of study serum level of Alanin aminotransferase (ALT), Aspartate aminotransferase (AST), Renin activity, Tumor necrosis factor- alpha (TNF- Ü), Liver tissues intercellular adhesion molecule-1 (ICAM-1), Angiotensinogen, TNF- Ü and Interleukin- 10 (IL-10) and Tracheal tissues angiotensin type- 1 receptors (AT1R), angiotensin type- 2 receptors (AT2R), muscarinic receptors, TNF- Ü and IL-10 were measured