皮细胞增加NO合成而发挥药理作用［7］。L-Arg在一氧化氮合成酶(NOS)催化下，产生NO，NO可直接弥散至血管平滑肌细胞，与之结合，激活鸟苷酸环化酶，增加细胞内cGMP浓度，促进Na+-Ca2+转换，使平滑肌松驰，扩张血管。而缺血缺氧肺血管收缩，已被证实L-Arg能够降低缺氧性肺动脉高压，其次L-Arg可以增加内皮细胞抗中性粒细胞(PMN)粘附作用，避免其粘附活化释放有害物质，从而保护肺组织细胞，实验中观察到Arg组肺毛细血管、肺间质及肺胞腔内无明显PMN聚集现象，
再者NO能够直接进入血小板，增加cGMP，导致血小板活性降低，聚集力下降，另一方面NO也可抑制PMN释放血小板活化因子使血小板活性减低，从而避免血栓形成。许多实验表明静滴L-Arg可使血浆中的内皮素浓度下降［8］，ET是体内已知缩血管作用最强的物质，肺血管平滑肌和支气管平滑肌细胞均有大量ET受体，缺血缺氧，ET合成增加，使肺血管强烈收缩和支气管痉挛，L-Arg通过增加NO合成抑制ET生成，从而扩张肺动脉，舒张支气管，改善通气/血流比值，提高氧合能力。 参考文献
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