Objective To compare the effects of heparin versus urokinase injection intrapleurally in the management of pleural thickening and adhesion due to tuberculous exudative pleurisy. Methods Sixty patients with tuberculous pleurisy were allocated into three groups randomly. Sodium heparin ( heparin group) , urokinase ( urokinase group) , and 0. 9% saline ( control group) were intrapleurally injected respectively. The concentrations of fibrinogen and D-dimer in pleural effusion were measured before and after the injection. The duration of absorption and the total drainage volume of pleural effusion were recorded. The pleural thickness and adhesion were observed two months after the injection. Results In 72 hours after the intrapleural injection, the concentration of fibrinogen( g/L) in the pleural effusion was significantly increased in the heparin group( 1. 13 ±0. 44 vs 0. 34 ±0. 19, P lt; 0. 001) , and significantly decreased in the urokinase group( 0. 25 ±0. 16 vs 0. 38 ±0. 15, P lt; 0. 05) when compared with baseline. Concentrations of D-dimer in the pleural effusions were significantly higher than those at baseline in both the heparin group and the urokinase group( 57. 0 ±17. 6 vs 40. 0 ±15. 4, P lt; 0. 05; 74. 5 ±16. 4 vs 43. 8 ±14. 9, P lt; 0. 001) . There were no significant differences in the absorption duration of pleural effusion among the three groups( P gt;0. 05) . The total drainage volume of pleural effusion was higher in the heparin group and the urokinase group compared to the control group( P lt;0. 01) . And the total volume of pleural effusion was significantly higher in the heparin group and the urokinase group than that in the control group( 2863 mL and 2465 mL vs 1828 mL,P lt;0. 01) . Two months after the intervention, the pleura were thinner[ ( 1. 37 ±0. 82) mm and ( 1. 33 ±0. 85) mmvs ( 3. 06 ±1. 20) mm, P lt; 0. 01] and the incidence of pleural adhesion was significantly lower[ 15% and 20% vs 50% , P lt; 0. 05] in the heparin and the urokinase groups than those in the control group.Conclusion Intrapleural heparin has similar effects with urokinase for prevention pleural thickness andadhesion in tuberculous pleurisy with good availability and safety.
Objective To improve the flexibil ity and hemostatic properties of chitosan (CS)/carboxymethyl chitosan (CMCS) hemostatic membrane by using glycerol and etamsylate to modify CS/CMCS hemostatic membrane. To investigate themechanical properties and hemostatic capabil ity of modified CS/CMCS hemostatic membrane. Methods The 2% CS solution, 2% CMCS solution, 10%, 15%, 20%, 25%, 30% glycerol with or without 0.5% etamsylate were used to prepare CS/CMCS hemostatic membrane with or without etamsylate by solution casting according to ratio of 16 ∶ 4 ∶ 5. The tensile properties were evaluated by tensile test according to GB 13022-1991. Twenty venous incisions and five arterial incisions hemorrhage of 1 cm × 1 cm in rabbit ears were treated by CS/CMCS hemostatic membrane modified by 15% (group A) and 25% (group B) of glycerol, and a combination of them and 0.5% etamsylate (groups C and D). The bleeding time and blood loss were recorded. Results The pH of yellow CS/ CMCS hemostatic membrane with thickness of 30-50 μm was 3-4. The incorporation glycerol into CS/CMCS hemostatic membrane resulted in decreasing in tensile strength (7.6%-60.2%) and modulus (97%-99%). However, elongation at break and water content increased 5.7-11.6 times and 13%-125% markedly. CS/CMCS hemostatic membrane adhered to wound rapidly, absorbed water from blood and became curly. The bleeding time and blood loss of venous incisions were (70 ± 3) seconds and (117.2 ± 10.8) mg, (120 ± 10) seconds and (121.2 ± 8.3) mg, (52 ± 4) seconds and (98.8 ± 5.5) mg, and (63 ± 3) seconds and (90.3 ± 7.1) mg in groups A, B, C, and D, respectively; showing significant differences (P lt; 0.05) between groups A, B and groups C, D. The bleeding time and blood loss of arterial incision were (123 ± 10) seconds and (453.3 ± 30.0) mg in group C. Conclusion CS/CMCS hemostatic membrane modified by glycerol and etamsylate can improve the flexibil ity, and shorten the bleeding time.
ObjectiveTo investigate the protecting effect of rosiglitazone for lung in airway-instillation- lipopolysaccharides and smoke-induced chronic obstructive pulmonary disease (COPD) rat models.MethodsFifty male Wistar rats with the SPF standard were randomly divided into 5 groups (n=10). The rats were treated by airway-instillation-lipopolysaccharides and exposing to smoking to establish COPD rat models excepted normal group, and the treatment groups were received gavage rosiglitazone of 0.1 mg/kg, 0.15 mg/kg, and 0.2 mg/kg rosiglitazone daily for 30 days, and the normal group or model group was received gavage normal saline. All rats were sacrificed after 30 days' treatment, and the lung tissue section was stained by hematoxylin and eosin. The mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured in all groups. In addition, the protein levels of p-Stat3 and p-NF-κB were detected by immunohistochemistry.ResultsCompared with normal group, the inflammation and emphysema were observed in the lung of rats in model group, and the symptoms of the group treated with rosiglitazone were lighter than normal group. The lungs of rats treated with highest dose of rosiglitazone (0.2 mg/kg) were evaluated with lowest pathology assessment score among three treatment groups, but there was no significant difference of MLI or MAN among three treatment groups. Compared with normal group, the protein levels of p-Stat3 and p-NF-κB were increased in the lung and tracheal epithelium and lymphoid tissue of rats in model group, while the protein levels of p-NF-κB were decreased in these tissues and the protein levels of p-Stat3 were decreased in the lymphoid tissue after treatment with rosiglitazone, but the protein levels of p-Stat3 were not changed in the lung and tracheal epithelium.ConclusionRosiglitazone has a protective effect on the COPD rat models by inhibiting NF-κB pathway to reduce the inflammation of the lung parenchyma.