吸入性一氧化氮 (NO)作为一种选择性肺血管扩张剂而应用于临床 ,然而 ,当NO吸入撤离后 ,可出现肺动脉压急剧升高的反跳现象 ,称为反跳性肺高压。近年来的研究认为反跳性肺高压可能是在内皮素的参与下 ,外源性的NO抑制了内源性一氧化氮合酶的活性或环鸟苷酸特异性的磷酸二酯酶增多了 ,导致体内的血管收缩因子超过了舒张因子 ,使肺血管阻力增高。逐步降低NO的吸入浓度再撤离或者联合应用潘生丁治疗可能会减轻反跳性肺高压的程度 Inhaled nitric oxide (NO) is used clinically as a selective pulmonary vasodilator. However, when NO is aspirated and evacuated, a sharp rebound in pulmonary arterial pressure may occur, called rebound pulmonary hypertension. In recent years, studies suggest that the rebound pulmonary hypertension may be endothelin-induced exogenous NO inhibited the activity of endogenous nitric oxide synthase or cyclic guanosine monophosphate-specific phosphodiesterase increased , Leading to the body’s vasoconstriction factor over the relaxation factor, so that pulmonary vascular resistance increased. Gradual reduction of inhaled concentrations of NO followed by withdrawal or dipyridamole treatment may reduce the degree of rebound pulmonary hypertension