2003PubMedRequires access

[Protective effect of a protease inhibitor on acute lung injury after hepatic ischemia/reperfusion in the rat].

Xiaolin Wang, Hong Zhang, Rong Liu, Hemei Wang

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Abstract

OBJECTIVE: To study the role of a protease inhibitor (ulinastatin) in protection of lung damage following hepatic ischemia/reperfusion in rat. METHODS: Thirty-two healthy male SD rats were randomly divided into four groups (n=8 in each group). Group A was served as sham-injury control group, group B rats were subjected to 90 minutes hepatic ischemia, and group C rats underwent 120 minutes reperfusion after 90 minutes ischemia of the liver. Ulinastatin (UTI) was administered to animals in group D which were reperfused 120 minutes after 90 minutes of ischemia of the liver. In addition to plasma malondialdehyde (MDA), broncho-alveolar lavage fluid protein (BALFP) content, and lung dry-to-wet weight ratios (D/W) were respectively examined in each group. The concentration of myeloperoxidase (MPO) in lung tissue was also measured. RESULTS: Compared to group A, plasma MDA, content of MPO in lung tissues and BALFP were significantly increased in both group B and group C, but they were much lower than those in group D. In addition, D/W was markedly decreased during hepatic ischemia and after 120 minutes reperfusion, while it was significantly increased in animals pretreated with UTI. CONCLUSION: Acute lung injury after hepatic ischemia and reperfusion is mainly induced by the oxidant stress, and neutrophil infiltration in the lung tissues is responsible for the damage under these conditions. Proteases inhibitors such as UTI might have antioxidation effects which attenuate lung injury induced by trauma to remote organs.

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OBJECTIVE: To study the role of a protease inhibitor (ulinastatin) in protection of lung damage following hepatic ischemia/reperfusion in rat. METHODS: Thirty-two healthy male SD rats were randomly divided into four groups (n=8 in each group). Group A was served as sham-injury control group, group B rats were subjected to 90 minutes hepatic ischemia, and group C rats underwent 120 minutes reperfusion after 90 minutes ischemia of the liver. Ulinastatin (UTI) was administered to animals in group D which were reperfused 120 minutes after 90 minutes of ischemia of the liver. In addition to plasma malondialdehyde (MDA), broncho-alveolar lavage fluid protein (BALFP) content, and lung dry-to-wet weight ratios (D/W) were respectively examined in each group. The concentration of myeloperoxidase (MPO) in lung tissue was also measured. RESULTS: Compared to group A, plasma MDA, content of MPO in lung tissues and BALFP were significantly increased in both group B and group C, but they were much lower than those in group D. In addition, D/W was markedly decreased during hepatic ischemia and after 120 minutes reperfusion, while it was significantly increased in animals pretreated with UTI. CONCLUSION: Acute lung injury after hepatic ischemia and reperfusion is mainly induced by the oxidant stress, and neutrophil infiltration in the lung tissues is responsible for the damage under these conditions. Proteases inhibitors such as UTI might have antioxidation effects which attenuate lung injury induced by trauma to remote organs.

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Available abstract

OBJECTIVE: To study the role of a protease inhibitor (ulinastatin) in protection of lung damage following hepatic ischemia/reperfusion in rat. METHODS: Thirty-two healthy male SD rats were randomly divided into four groups (n=8 in each group). Group A was served as sham-injury control group, group B rats were subjected to 90 minutes hepatic ischemia, and group C rats underwent 120 minutes reperfusion after 90 minutes ischemia of the liver. Ulinastatin (UTI) was administered to animals in group D which were reperfused 120 minutes after 90 minutes of ischemia of the liver. In addition to plasma malondialdehyde (MDA), broncho-alveolar lavage fluid protein (BALFP) content, and lung dry-to-wet weight ratios (D/W) were respectively examined in each group. The concentration of myeloperoxidase (MPO) in lung tissue was also measured. RESULTS: Compared to group A, plasma MDA, content of MPO in lung tissues and BALFP were significantly increased in both group B and group C, but they were much lower than those in group D. In addition, D/W was markedly decreased during hepatic ischemia and after 120 minutes reperfusion, while it was significantly increased in animals pretreated with UTI. CONCLUSION: Acute lung injury after hepatic ischemia and reperfusion is mainly induced by the oxidant stress, and neutrophil infiltration in the lung tissues is responsible for the damage under these conditions. Proteases inhibitors such as UTI might have antioxidation effects which attenuate lung injury induced by trauma to remote organs.

Key concepts: Ulinastatin, Medicine, Lung, Malondialdehyde, Ischemia, Myeloperoxidase, Reperfusion injury, Anesthesia

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[Protective effect of a protease inhibitor on acute lung injury after hepatic ischemia/reperfusion in the rat]. — Research Paper | ScholarLens