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据报道一氧化氮(NO)属于上皮源性松弛因子,大量研究探讨了吸入NO 对实验性及临床肺动脉高压的肺血管扩张作用.支气管树上皮细胞通过分泌一种上皮源性松弛因子(EpDRF)调节气道张力,但有研究显示NO 不同于EpDRF.而产生NO 的硝普钠有扩张羊支气管作用.作者用乙酰甲胆碱(MCh)诱发的支气管狭窄模型观察了NO 的作用.8只新西兰白兔经安定麻醉,利多卡因喷雾后气管插管人工呼吸,调整呼吸频率约30次/分,保持呼气末CO_2分压(PETCO_2)约5kPa,膨胀压(Pmax)在20cmH_2O 内,稳定30分钟后雾化吸入溶解的
It has been reported that nitric oxide (NO) is an epithelial-derived relaxing factor and a large number of studies have investigated the pulmonary vasodilatation effect of inhaled NO on experimental and clinical pulmonary hypertension. Bronchial epithelial cells, through the secretion of an epithelial-derived relaxing factor (EpDRF) Regulate airway tension, but studies have shown that NO is different from EpDRF, while nitric oxide, sodium nitroprusside, has the effect of expanding the bronchus of the sheep.The role of NO was observed in a model of bronchoconstriction induced by methacholine (MCh) .8 New Zealand The anesthetized rabbits were anesthetized and anesthetized with lidocaine. The lidocaine was sprayed for artificial respiration after intubation. The respiratory rate was adjusted to about 30 beats / min. The PETCO_2 was maintained at about 5kPa and the Pmax was stable within 20cmH_2O Inhalation dissolved in minutes after inhalation