Dinh-Xuan A T
Laboratoire de Physiologie Respiratoire, Faculté de Médecine Cochin Port-Royal Hôpital Cochin, Paris, France.
Eur Respir J. 1992 Jun;5(6):757-62.
Pulmonary endothelial cells normally synthesize prostacyclin (PGI2) and nitric oxide (NO), which are both potent vasodilators. Although PGI2 is largely used to treat patients with severe pulmonary hypertension, its role in the physiology and pathophysiology of the pulmonary circulation is still debated. NO, which is now considered as the endogenous nitrovasodilator, is perhaps more involved than PGI2 in the mechanisms that modulate pulmonary vascular tone in health and disease. There is evidence to suggest that background release of NO contributes to the normally low pulmonary vascular tone in normoxia. Although there are theoretical grounds to hypothesize that hypoxia reduces the synthesis of NO, lack of the latter does not seem to account for the acute hypoxic pulmonary vasoconstriction. Instead, there is evidence to suggest that NO activity is increased in order to modulate the pulmonary vasopressor response to acute alveolar hypoxia. However, more consistent, concerning the role of NO, are data gathered from studies performed in chronic hypoxic conditions. Both experimental data and studies performed in man demonstrate impairment of NO synthesis and/or release in chronic hypoxic pulmonary hypertension. The impaired NO production, whilst reducing the ability of the pulmonary vasculature to relax, also favours the occurrence of excessive pulmonary vasoconstriction. Lack of NO synthesis might also permit mitogenesis and proliferation of various cell types within the vascular wall. We hypothesize that functional alterations of pulmonary endothelium are likely to affect both reactivity and growth of pulmonary vessels. In this respect, NO probably has a pivotal role in modulating pulmonary vascular tone and controlling pulmonary vascular remodelling in health and disease.
肺内皮细胞通常合成前列环素（PGI2）和一氧化氮（NO），二者均为强效血管舒张剂。尽管PGI2在很大程度上用于治疗重度肺动脉高压患者，但其在肺循环生理和病理生理中的作用仍存在争议。NO现在被认为是内源性硝基血管舒张剂，在健康和疾病状态下调节肺血管张力的机制中，它可能比PGI2发挥着更重要的作用。有证据表明，在常氧状态下，NO的基础释放有助于维持正常较低的肺血管张力。虽然有理论依据推测缺氧会减少NO的合成，但后者的缺乏似乎并不能解释急性低氧性肺血管收缩。相反，有证据表明，为了调节肺血管对急性肺泡缺氧的升压反应，NO的活性会增加。然而，关于NO的作用，从慢性低氧条件下进行的研究中收集到的数据更为一致。实验数据和在人体中进行的研究均表明，在慢性低氧性肺动脉高压中，NO的合成和/或释放受损。NO生成受损，在降低肺血管舒张能力的同时，也有利于过度肺血管收缩的发生。NO合成的缺乏还可能使血管壁内各种细胞类型发生有丝分裂和增殖。我们推测，肺内皮的功能改变可能会影响肺血管的反应性和生长。在这方面，NO可能在健康和疾病状态下调节肺血管张力和控制肺血管重塑中起关键作用。
