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本文研究吸烟时大鼠血流动力学及缺氧性肺血管收缩反应(HPV)的变化及前列腺素(PGs)与白三烯(LTs)在其中的作用。实验发现,吸烟时体、肺血管阻力分别增加47%、39%,血浆与肺组织TXB_2浓度分别增加144%与69%。吸烟后HPV增强一倍(△PVR从55%增至102%)。白三烯受体阻断剂LY-171883可消除吸烟导致的体,肺血管阻力增加和HPV增强,环氧酶抑制剂消炎痛也可减轻吸烟引起的肺血管收缩,但对HPV的变化无影响。结果表明,吸烟可通过LTs导致体、肺血管收缩及HPV增强,吸烟时肺血管收缩还与TXA_2有关。本文还发现,LY-171883抑制HPV 72%,这表明LTs介导HPV。
This article studies the changes of hemodynamics and hypoxic pulmonary vasoconstriction (HPV) and the roles of prostaglandins (PGs) and leukotrienes (LTs) during smoking in rats. Experiments found that smoking body, pulmonary vascular resistance increased by 47%, 39%, plasma and lung tissue TXB_2 concentrations increased by 144% and 69%. After smoking, HPV doubled (△ PVR increased from 55% to 102%). LY-171883, a leukotriene receptor blocker, can eliminate smoking-induced increases in body and pulmonary vascular resistance and increase HPV, and cyclooxygenase inhibitor indomethacin can also reduce smoking-induced pulmonary vasoconstriction but has no effect on HPV changes . The results showed that smoking can lead to body, pulmonary vasoconstriction and HPV enhancement through LTs, while pulmonary vasoconstriction during smoking is also related to TXA_2. We also found that LY-171883 inhibits 72% of HPV, suggesting that LTs mediate HPV.