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本课题采用离体肺灌流方法,观察吸烟对肺血管基础阻力和缺氧性肺血管收缩反应的影响及其与前列腺素(PGs)和白三烯(LTs)的关系。结果表明短暂吸烟对离体灌流大鼠肺血管基础阻力没有影响,但可使其缺氧性肺血管收缩反应(HPV)加强。在灌流血液中加入消炎痛(20μg/ml血)后,可增强HPV,但吸烟后的HPV与对照组无明显差异。在灌流血液中加入乙胺嗪(1mg/ml血)后,吸烟前和吸烟后肺之HPV均明显低于对照组。联合应用消炎痛和乙胺嗪后,吸烟前和吸烟后的HPV均低于对照组。结果提示在HPV中LTs介导肺血管收缩,PGs限制肺血管收缩而起调节作用,吸烟可加强HPV、LTs在其中起介导作用。
In this study, the effect of smoking on pulmonary vascular resistance and hypoxic pulmonary vasoconstriction and its relationship with prostaglandin (PGs) and leukotrienes (LTs) were investigated by means of isolated pulmonary perfusion. The results showed that short-term smoking on perfused rat pulmonary vascular base resistance has no effect, but can make its hypoxic pulmonary vasoconstriction (HPV) increased. Adding indomethacin (20 μg / ml) to the perfusion blood increased HPV, but there was no significant difference between the HPV and control groups after smoking. Addition of diethylcarbamazine (1 mg / ml blood) to perfused blood resulted in significantly lower HPV levels in the lungs before and after smoking than in the control group. After combined application of indomethacin and diethylcarbamazine, HPV levels before and after smoking were lower than those in the control group. The results suggest that LTs mediate pulmonary vasoconstriction in HPV, PGs regulate pulmonary vasoconstriction and play a regulatory role, smoking can enhance HPV, LTs play a mediating role in them.