Moloney E D, Evans T W
Imperial College School of Medicine, Royal Brompton Hospital, London, UK.
Eur Respir J. 2003 Apr;21(4):720-7. doi: 10.1183/09031936.03.00120102.
Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance. Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit. Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.
肺动脉高压（PH）是急性呼吸窘迫综合征（ARDS）的一个特征性表现。已表明PH的严重程度与ARDS患者的肺损伤严重程度相关，且独立于相关低氧血症的严重程度，具有不良预后意义。在ARDS的组织病理学演变早期，肺血管收缩、血栓栓塞和间质水肿促成了PH的发展，尽管最终可能会发生肺血管重塑。静脉血管扩张剂会导致肺内分流增加和全身性低血压，这可能会限制其治疗用途，且尚未证明能改善生存率。相比之下，吸入给药的快速代谢血管扩张剂可诱导选择性肺血管扩张并减少分流，但同样似乎未带来生存获益。旨在进一步了解作为急性呼吸窘迫综合征特征性表现的肺动脉高压潜在机制的研究，有望改善急性呼吸窘迫综合征中肺动脉高压的药物干预措施。
