Effect of nitric oxide on lung injury induced by total hepatic ischemia-reperfusion in rats
Chang Ye-tian
Abstract
Chang Ye-tian
Abstract
Objectives To evaluate effects of nitric oxide(NO)on lung injury following total hepatic ischemia-reperfusion(I/R) in rats. Methods The total hepatic ischemia-reperfusion model was made by the blocks of hepatic porta, suprahepatic and infrahepatic vena cava for 20 min. sixty Sprague- Dawaley rats were divided randomly into three groups: Sham operation group (group A n =20), total hepatic ischemia-reperfusion group (group B n =20), and aminoguanidine treatment group. (group C n =20). Each group was subdivided randomly into two subgroups (n =10) according to different experiment time point as follows: at the end of the 20min total hepatic ischemia (T0), 4 h after reperfusion (T1), Group A and Group B were received normal saline (1 ml/kg) while group C was received aminoguanidine 20 mg/kg which was dissolved in 1ml/kg of normal saline 10min before abdominal open intravenously. The contents of NO in portal vein blood and lung, the wet/dry and the morphological changes of the lungs were examined. Results Compared with group A, the contents of NO in portal venous blood and lung at T1 in group B and group C increased significantly, and the wet/dry of the lung in group B and group C at T1 was significantly higher (P 0.01). The lung morphological change in group C was less than that in group B while no obviously morphological change was founded in group A. Conclusion Nitric oxide may play an important role in acute lung injury induced by the total hepatic ischemia-reperfusion in rats.
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Objectives To evaluate effects of nitric oxide(NO)on lung injury following total hepatic ischemia-reperfusion(I/R) in rats. Methods The total hepatic ischemia-reperfusion model was made by the blocks of hepatic porta, suprahepatic and infrahepatic vena cava for 20 min. sixty Sprague- Dawaley rats were divided randomly into three groups: Sham operation group (group A n =20), total hepatic ischemia-reperfusion group (group B n =20), and aminoguanidine treatment group. (group C n =20). Each group was subdivided randomly into two subgroups (n =10) according to different experiment time point as follows: at the end of the 20min total hepatic ischemia (T0), 4 h after reperfusion (T1), Group A and Group B were received normal saline (1 ml/kg) while group C was received aminoguanidine 20 mg/kg which was dissolved in 1ml/kg of normal saline 10min before abdominal open intravenously. The contents of NO in portal vein blood and lung, the wet/dry and the morphological changes of the lungs were examined. Results Compared with group A, the contents of NO in portal venous blood and lung at T1 in group B and group C increased significantly, and the wet/dry of the lung in group B and group C at T1 was significantly higher (P 0.01). The lung morphological change in group C was less than that in group B while no obviously morphological change was founded in group A. Conclusion Nitric oxide may play an important role in acute lung injury induced by the total hepatic ischemia-reperfusion in rats.
Key concepts: Medicine, Nitric oxide, Lung, Saline, Reperfusion injury, Group B, Ischemia, Group A