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

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.

[The experimental study of therapeutical effects of KANGFUXINYE on upper gastrointestinal injury induced by paraquat in rats].

OBJECTIVE: To investigate the therapeutical effects of KANGFUXINYE on the upper gastrointestinal injury induced by paraquat in rats, and to explore the proper mechanism. METHODS: A total of 120 adult Wistar male rats were randomly divided into three groups, control group (CG), model group (MG) and treatment group (TG), 40 rats each group. The MG and TG were given 20% paraquat 50 mg/kg by oral administration, after 2 h the TG was given KANGFUXINYE solution 1.5 ml by oral administration, 3 times a day. The CG was given normal saline. On the 3rd, 6th, 9th, 12th and 15th days after exposure, 8 rats of each group were killed respectively, and the tissues from esophagus and stomach were collected and examined by HE staining for observing the mucosa injury. The superoxide dismutase (SOD) and malondialdehyde (MDA) of serum were detected. RESULTS: On the 3rd, 6th, 9th, 12th and 15th days after exposure, the results of pathological examination showed that the mucosa injury in TG was significantly relieved as compared with MG, the activity of serum SOD reduced obviously and the MDA levels increased significantly in MG, as compared with CG (P<0.05). The activity of serum SOD increased obviously and the MDA levels decreased significantly in TG, as compared with MG (P<0.05). CONCLUSION: The results of present indicate that KANGFUXINYE has the therapeutical effects on the upper gastrointestinal injury caused by paraquat in rats. The mechanism of therapeutical effects may be due to the increasing SOD activity, eliminating free radicles and inhibiting the lipid peroxidation.

[Experimental therapy of penehyclidine hydrochloride on paraquat-induced acute lung injury].

OBJECTIVE: To observe the therapeutic effect and mechanism of penehyclidine hydrochloride on paraquat-induced acute lung injury. METHODS: 80 healthy adult male Wistar rats were randomly assigned into control groups (10 rats), 100 mg/kg PQ group (10 rats), 100 mg/kg PQ plus 33 µg/kg penehyclidine hydrochloride treatment group (30 rats), 100 mg/kg PQ plus 66 µg/kg penehyclidine hydrochloride treatment group (30 rats). The two treatment groups were executed respectively at 36 h, 72 h and 7 d. Lung tissues were used to assess histopathological change by HE staining. The level of MMP-2, caveolin-1 and HYP were detected in the lung homogenate. The serum and BALF contents of ET were measured. RESULTS: Pathology inspection confirmed that the model of acute rat pulmonary injury were duplicated successfully. The level of MMP-2, HYP in lung tissues and the serum and BALF ET contents in PQ group were (1.77 ± 0.40) µg/g, (2.91 ± 0.79) µg/g, (505.23 ± 124.69) µg/ml, (640.38 ± 136.60) µg/ml. The level of those was higher than that in control group [(0.95 ± 0.66) µg/g, (1.48 ± 0.69) µg/g, (95.48 ± 46.01) µg/ml, (200.40 ± 88.39) µg/ml, P < 0.05]; The above-mentioned index in two treatment groups was lower than that in PQ group (P < 0.05). The caveolin-1 content [(1.77 ± 0.82) µg/g] in PQ group was lower than that in control group [(5.39 ± 1.68) µg/g, P < 0.05]. The level of caveolin-1 in two treatment groups was higher than that in PQ group (P < 0.05). CONCLUSION: Penehyclidine hydrochloride can decrease the level of MMP-2, HYP in lung tissues and the ET in serum and BALF, increase that of caveolin-1 and lessen the damage induced by paraquat.