摘要
目的:从肺组织中TXB2和6-Keto-PGF1!含量的变化,探讨不同浓度艾烟对小鼠肺组织及肺微循环的影响。方法:设立不同浓度的艾烟环境烟熏小鼠,用光学显微镜作病理观察,ELISA法测定TXB2和6-Keto-PGF1!水平。结果:肺组织病理观察结果显示,中浓度组出现渗出性炎症,高、低浓度组未见异常;中浓度组TXB-2含量降低,具有统计学意义(P<0.05),高、低浓度组含量有降低趋势,但均无统计意义(P>0.05);6-Keto-PGF1!含量中浓度组增高,具有统计学意义(P<0.05),高、低浓度组含量有降低趋势,但均无统计意义(P>0.05)。结论:艾烟促进PGI2的表达,抑制TXA2的表达。这可能与肺组织的缺氧、血小板聚集、微血栓形成等因素引起血管内皮细胞受刺激,反应性引起PGI2生成释放有关。一方面有利于加快局部渗出液的吸收,改善肺微循环环境,促进肺组织炎症的恢复。另一方面过度的血管扩张和抑制血小板聚集会导致肺内充血和出血的发生。
Objective: To study the effect of Moxa-smog to Mouse lung and lung microcirculation from TXB2 and 6-Keto-PGF1 aiM lung in different Moxa-smog environment. Methods: We simulated the different Moxa-smog environment and optical microscope to observe the index of pathology, ELISA measuring TXB2 and 6-Keto-PGF1 ctlevel in lung. Results: There were Bronchitis, congestion and bronchial in the middle concentration group. Compared with the control group, There was no statistical significance in the lower concentration group and the high concentration group (P 〉 0. 05) ; the middle concentration group decreased, with significant difference ( P 〈 0. 05 ) . Compared with the control group, there was no statistical significance in the lower concentration group and the high concentration group (P 〉 0. 05 ) ; the middle concentration group increased, with significant difference ( P 〈 0. 05 ) . Conclusion: After smoked, the expression of TXA2 and PGI2 at a low level equilibrium in no pathological changes occurred of the mouse. The body regulatory function decline for pulmonary vascular and airway. Moxa-smog can promote the expression of TXA2 and Inhibit the expression of PGI2. This may be the mechanisms of leading pulmonary vascular and bronchial edema. Moxa-smog can promote the expression of PGI2 and inhibit the expression of TXA2. This may be the mechanisms of leading lung congestion and bronchial bureaucratic of bleeding.
出处
《成都中医药大学学报》
2014年第3期31-33,共3页
Journal of Chengdu University of Traditional Chinese Medicine
关键词
艾烟
浓度
病理
肺微循环
Moxa-smog
concentration
pathology
lung microcirculation