摘要
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。
Isolated rat lungs perfused with blood were used to determine the effects of cigarette smoke delivered into the lung by a ventilator on the pulmonary vascular resistance(PVR), and on the hypoxic pulmonary vasoconstriction (HPV), and to explore the roles that prostaglandin and leukotrienes played in that effect. The results showed that the PVR did not change, while the HPV was significantly enhanced by smoking. Indomethacin an inhibitor of PGs biosynthesis administered in the perfused blood(20μg/ml)increased HPV in non-smoking lungs, but not in lungs after smoking. Diethylcarbamazine Citrate (DEC, 1mg/ml), an inhibitor of LTs biosynthesis, decreased the HPV before and after smoking. After perfusing indomethacin combined with DEC the HPV also decreased. It is suggested that leukotrienes act as mediators in HPV whereas prostaglandins as modulators, LTs might play an important role in the increase of HPV by cigarette smoking.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1990年第3期133-136,共4页
Chinese Journal of Pathophysiology
基金
国家"七五"攻关课题
关键词
吸烟
肺
血管收缩
前列腺素类
Smoking
Lung, vasoconstriction
Prostaglandins
