2012PubMedRequires access

[Experimental anticoagulant therapy of acute lung injury induced by paraquat].

Feng Liu, Xiangdong Jian, Zhongchen Zhang, Huimin Liu, Qian Zhou, Wei Zhang, Bo Z. Shang, Dong Tian, Yan-ying Niu, Yan-qun Bi, Jian Xin Jiang

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Abstract

OBJECTIVE: To establish a model of acute lung injury induced by paraquat poisoning and to observe the effects of anticoagulant therapy on acute lung injury induced by paraquat poisoning. METHODS: One hundred twenty adult healthy male Wistar rats were randomly divided into three groups: the paraquat poisoning group was exposed intragastrically (IG) to 50 mg/kg paraquat, anticoagulant therapy group was exposed intragastrically (IG) to 50 mg/kg paraquat then administrated subcutaneously with 68 U/kg low molecular heparin calcium 2 times a day and administrated intragastrically with 1.67 mg/kg aspirin one tome a day for 3, 7, 14 and 21 days, respectively, control group exposed intragastrically to normal saline. After exposure the rats were sacrificed, the venous blood and lung tissues were collected to detect the prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin time and D-dimer in blood and the hydroxyproline in lung tissues, and to examine pathological changes in lung tissues with HE and Masson staining under light microscope. RESULTS: At the 3rd, 7th, 14th and 21st days after exposure, the hydroxyproline contents of lung tissues in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), but the hydroxyproline contents of lung tissues in anticoagulation therapy group were significantly lower than those in paraquat poisoning group (P < 0.05). At the 3rd day after exposure, the PT, APTT, Fib and D-dimer levels in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), the D-dimer level of anticoagulation therapy group was significantly lower than that of control group (P < 0.05). At the 7th, 14th and 21st days after exposure, the TT and D-dimer levels of paraquat poisoning group and anticoagulation therapy group were significantly higher than those of control group (P < 0.05), the TT and D-dimer levels of anticoagulation therapy group were significantly lower than those of paraquat poisoning group (P < 0.05). The lung injury in paraquat poisoning group increased with exposure period, the lung fibrosis in anticoagulation therapy group was lower than that in paraquat poisoning group. CONCLUSION: Anticoagulation therapy can improve hyper-coagulation state and acute lung injury in rats induced by paraquat poisoning.

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What this paper is about

OBJECTIVE: To establish a model of acute lung injury induced by paraquat poisoning and to observe the effects of anticoagulant therapy on acute lung injury induced by paraquat poisoning. METHODS: One hundred twenty adult healthy male Wistar rats were randomly divided into three groups: the paraquat poisoning group was exposed intragastrically (IG) to 50 mg/kg paraquat, anticoagulant therapy group was exposed intragastrically (IG) to 50 mg/kg paraquat then administrated subcutaneously with 68 U/kg low molecular heparin calcium 2 times a day and administrated intragastrically with 1.67 mg/kg aspirin one tome a day for 3, 7, 14 and 21 days, respectively, control group exposed intragastrically to normal saline. After exposure the rats were sacrificed, the venous blood and lung tissues were collected to detect the prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin time and D-dimer in blood and the hydroxyproline in lung tissues, and to examine pathological changes in lung tissues with HE and Masson staining under light microscope. RESULTS: At the 3rd, 7th, 14th and 21st days after exposure, the hydroxyproline contents of lung tissues in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), but the hydroxyproline contents of lung tissues in anticoagulation therapy group were significantly lower than those in paraquat poisoning group (P < 0.05). At the 3rd day after exposure, the PT, APTT, Fib and D-dimer levels in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), the D-dimer level of anticoagulation therapy group was significantly lower than that of control group (P < 0.05). At the 7th, 14th and 21st days after exposure, the TT and D-dimer levels of paraquat poisoning group and anticoagulation therapy group were significantly higher than those of control group (P < 0.05), the TT and D-dimer levels of anticoagulation therapy group were significantly lower than those of paraquat poisoning group (P < 0.05). The lung injury in paraquat poisoning group increased with exposure period, the lung fibrosis in anticoagulation therapy group was lower than that in paraquat poisoning group. CONCLUSION: Anticoagulation therapy can improve hyper-coagulation state and acute lung injury in rats induced by paraquat poisoning.

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Available abstract

OBJECTIVE: To establish a model of acute lung injury induced by paraquat poisoning and to observe the effects of anticoagulant therapy on acute lung injury induced by paraquat poisoning. METHODS: One hundred twenty adult healthy male Wistar rats were randomly divided into three groups: the paraquat poisoning group was exposed intragastrically (IG) to 50 mg/kg paraquat, anticoagulant therapy group was exposed intragastrically (IG) to 50 mg/kg paraquat then administrated subcutaneously with 68 U/kg low molecular heparin calcium 2 times a day and administrated intragastrically with 1.67 mg/kg aspirin one tome a day for 3, 7, 14 and 21 days, respectively, control group exposed intragastrically to normal saline. After exposure the rats were sacrificed, the venous blood and lung tissues were collected to detect the prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin time and D-dimer in blood and the hydroxyproline in lung tissues, and to examine pathological changes in lung tissues with HE and Masson staining under light microscope. RESULTS: At the 3rd, 7th, 14th and 21st days after exposure, the hydroxyproline contents of lung tissues in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), but the hydroxyproline contents of lung tissues in anticoagulation therapy group were significantly lower than those in paraquat poisoning group (P < 0.05). At the 3rd day after exposure, the PT, APTT, Fib and D-dimer levels in paraquat poisoning group and anticoagulation therapy group were significantly higher than those in control group (P < 0.05), the D-dimer level of anticoagulation therapy group was significantly lower than that of control group (P < 0.05). At the 7th, 14th and 21st days after exposure, the TT and D-dimer levels of paraquat poisoning group and anticoagulation therapy group were significantly higher than those of control group (P < 0.05), the TT and D-dimer levels of anticoagulation therapy group were significantly lower than those of paraquat poisoning group (P < 0.05). The lung injury in paraquat poisoning group increased with exposure period, the lung fibrosis in anticoagulation therapy group was lower than that in paraquat poisoning group. CONCLUSION: Anticoagulation therapy can improve hyper-coagulation state and acute lung injury in rats induced by paraquat poisoning.

Key concepts: Paraquat, Lung, Partial thromboplastin time, Medicine, Prothrombin time, Thrombin time, Hydroxyproline, Gastroenterology

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