2005Zhongguo Yike Daxue xuebaoRequires access

Protective effect of ischemia preconditioning on acute lung injury after hepatic ischemia/reperfusion

Wei-Min Chen

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Abstract

Objective: To investigate the mechanism of acute lung injury after hepatic ischemia/ reperfusion and the protective effect of ischemia preconditioning. Methods: Eighteen healthy Wistar rats weighting 240 to 280 g were randomly divided into 3 groups (6 in each group). Group I/R: the hepatic pedicle was clamped for 40 minutes with portal bypass and then opened for reperfusion which lasted for 3 hours. Group IP: the hepatic pedicle was clamped for 5 minutes and untied for 5 minutes and then ischemia reperfusion was produced as Group I/R. Group C: the hepatic pedicle was only exposed for 40 minutes. In addition to broncho-alveolar lavage fluid protein (BALFP) content, water content of lung tissue, and malondialdehyde (MDA) in serum and lung tissue were measured. The concentration of myeloperoxidase(MPO) in lung tissue was also examined. Results: Compared with group C, the BALFP and water content were significantly increased in Group I/R, but which were unmarkably increased in group IP. The content of MPO and MDA in lung tissue and serum MDA in group I/R were higher than those in group C and group IP. Preconditioning might decrease the improvement of MPO and MDA. Conclusion: Acute lung injury after hepatic ischemia/ reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues. Ischemia preconditioning may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia/ reperfusion.

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Objective: To investigate the mechanism of acute lung injury after hepatic ischemia/ reperfusion and the protective effect of ischemia preconditioning. Methods: Eighteen healthy Wistar rats weighting 240 to 280 g were randomly divided into 3 groups (6 in each group). Group I/R: the hepatic pedicle was clamped for 40 minutes with portal bypass and then opened for reperfusion which lasted for 3 hours. Group IP: the hepatic pedicle was clamped for 5 minutes and untied for 5 minutes and then ischemia reperfusion was produced as Group I/R. Group C: the hepatic pedicle was only exposed for 40 minutes. In addition to broncho-alveolar lavage fluid protein (BALFP) content, water content of lung tissue, and malondialdehyde (MDA) in serum and lung tissue were measured. The concentration of myeloperoxidase(MPO) in lung tissue was also examined. Results: Compared with group C, the BALFP and water content were significantly increased in Group I/R, but which were unmarkably increased in group IP. The content of MPO and MDA in lung tissue and serum MDA in group I/R were higher than those in group C and group IP. Preconditioning might decrease the improvement of MPO and MDA. Conclusion: Acute lung injury after hepatic ischemia/ reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues. Ischemia preconditioning may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia/ reperfusion.

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Available abstract

Objective: To investigate the mechanism of acute lung injury after hepatic ischemia/ reperfusion and the protective effect of ischemia preconditioning. Methods: Eighteen healthy Wistar rats weighting 240 to 280 g were randomly divided into 3 groups (6 in each group). Group I/R: the hepatic pedicle was clamped for 40 minutes with portal bypass and then opened for reperfusion which lasted for 3 hours. Group IP: the hepatic pedicle was clamped for 5 minutes and untied for 5 minutes and then ischemia reperfusion was produced as Group I/R. Group C: the hepatic pedicle was only exposed for 40 minutes. In addition to broncho-alveolar lavage fluid protein (BALFP) content, water content of lung tissue, and malondialdehyde (MDA) in serum and lung tissue were measured. The concentration of myeloperoxidase(MPO) in lung tissue was also examined. Results: Compared with group C, the BALFP and water content were significantly increased in Group I/R, but which were unmarkably increased in group IP. The content of MPO and MDA in lung tissue and serum MDA in group I/R were higher than those in group C and group IP. Preconditioning might decrease the improvement of MPO and MDA. Conclusion: Acute lung injury after hepatic ischemia/ reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues. Ischemia preconditioning may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia/ reperfusion.

Key concepts: Myeloperoxidase, Lung, Malondialdehyde, Medicine, Ischemia, Reperfusion injury, Infiltration (HVAC), Ischemic preconditioning

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