Cremona G, Dinh Xuan A T, Higenbottam T W
Department of Respiratory Physiology, Papworth Hospital, Cambridge, UK.
Lung. 1991;169(4):185-202. doi: 10.1007/BF02714154.
Endothelium-derived relaxing factor (EDRF) is probably identical to nitric oxide (NO) and is released by the vascular endothelium both in the basal unstimulated state and in response to a wide range of physical and chemical stimuli. Since it was first described 10 years ago, evidence is accumulating that it is an important modulator of vascular smooth muscle tone. EDRF acts on the pulmonary vascular bed as on the systemic circulation. EDRF release to pharmacologic stimuli is impaired in pulmonary arteries from patients with chronic hypoxemia. This impairment is associated with severity of respiratory failure and of structural change of vessel walls. Disturbance of EDRF activity may be important in the pathophysiology of pulmonary vascular disease. This brief review describes the current status of experimental studies concerning the possible role of EDRF on the pulmonary circulation in normal conditions and in the pathogenesis of pulmonary hypertension.
内皮源性舒张因子（EDRF）可能与一氧化氮（NO）相同，在基础未受刺激状态以及对多种物理和化学刺激作出反应时，由血管内皮释放。自10年前首次被描述以来，越来越多的证据表明它是血管平滑肌张力的重要调节因子。EDRF对肺血管床的作用与对体循环的作用相同。慢性低氧血症患者肺动脉中EDRF对药物刺激的释放受损。这种损害与呼吸衰竭的严重程度和血管壁结构改变有关。EDRF活性紊乱在肺血管疾病的病理生理学中可能很重要。这篇简短的综述描述了关于EDRF在正常情况下和肺动脉高压发病机制中对肺循环可能作用的实验研究现状。
