Liu Feng, Jian Xiang-dong, Zhang Zhong-chen, Liu Hui-min, Zhou Qian, Zhang Wei, Shang Bo, Tian Dong, Niu Yan-ying, Bi Yan-qun, Jiang Jian
Department of Poisoning and Occupational Diseases, Qilu Hospital of Shandong University, Jinan 250012, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012 Mar;30(3):190-3.
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.
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.
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.
Anticoagulation therapy can improve hyper-coagulation state and acute lung injury in rats induced by paraquat poisoning.
建立百草枯中毒致急性肺损伤模型,观察抗凝治疗对百草枯中毒致急性肺损伤的影响。
将120只成年健康雄性Wistar大鼠随机分为三组:百草枯中毒组经胃内给予50mg/kg百草枯;抗凝治疗组经胃内给予50mg/kg百草枯,然后皮下注射68U/kg低分子肝素钙,每天2次,并经胃内给予1.67mg/kg阿司匹林,每天1次,分别给药3、7、14和21天;对照组经胃内给予生理盐水。染毒后处死大鼠,采集静脉血和肺组织,检测血液中凝血酶原时间、活化部分凝血活酶时间、纤维蛋白原、凝血酶时间和D-二聚体以及肺组织中羟脯氨酸含量,并在光镜下用HE和Masson染色检查肺组织的病理变化。
染毒后第3、7、14和21天,百草枯中毒组和抗凝治疗组肺组织羟脯氨酸含量均显著高于对照组(P<0.05),但抗凝治疗组肺组织羟脯氨酸含量显著低于百草枯中毒组(P<0.05)。染毒后第3天,百草枯中毒组和抗凝治疗组PT、APTT、Fib和D-二聚体水平均显著高于对照组(P<0.05),抗凝治疗组D-二聚体水平显著低于百草枯中毒组(P<0.05)。染毒后第7、14和21天,百草枯中毒组和抗凝治疗组TT和D-二聚体水平均显著高于对照组(P<0.05),抗凝治疗组TT和D-二聚体水平显著低于百草枯中毒组(P<0.05)。百草枯中毒组肺损伤随染毒时间延长而加重,抗凝治疗组肺纤维化程度低于百草枯中毒组。
抗凝治疗可改善百草枯中毒大鼠的高凝状态和急性肺损伤。