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急性肺损伤中的肺循环:近期进展综述

The pulmonary circulation in acute lung injury: a review of some recent advances.

作者信息

Leeman M

机构信息

Department of Intensive Care, Erasme University Hospital, Brussels, Belgium.

出版信息

Intensive Care Med. 1991;17(5):254-60. doi: 10.1007/BF01713933.

Abstract
  1. According to the Starling resistor model of the pulmonary circulation, the pulmonary hypertension of oleic acid lung injury, an experimental model close to the early stage of clinical ARDS, primarily results from an increased vascular closing pressure which exceeds Pla and becomes the effective outflow pressure of the pulmonary circulation. Therefore, calculated pulmonary vascular resistance should be interpreted cautiously during haemodynamic investigations in patients with ARDS. 2. Part of this increased vascular closing pressure is functional. During acute lung injury pulmonary vasomotor tone can be reduced by vasodilators, or increased by cyclooxygenase inhibitors and almitrine. 3. Pulmonary vasodilation due to infused vasodilators usually impairs gas exchange in ARDS. 4. There is evidence that HPV is altered during ARDS. Drugs capable of enhancing the efficacy of HPV could improve gas exchange. If proven safe in the future, cyclooxygenase inhibitors and almitrine are interesting compounds to be tested in ARDS.
摘要
  1. 根据肺循环的斯塔林电阻器模型,油酸肺损伤(一种接近临床急性呼吸窘迫综合征早期的实验模型)的肺动脉高压主要源于血管闭合压升高,该压力超过肺泡压并成为肺循环的有效流出压。因此,在急性呼吸窘迫综合征患者的血流动力学研究中,计算得出的肺血管阻力应谨慎解读。2. 这种血管闭合压升高部分是功能性的。在急性肺损伤期间,血管扩张剂可降低肺血管运动张力,而环氧合酶抑制剂和阿米三嗪可增加肺血管运动张力。3. 输注血管扩张剂引起的肺血管扩张通常会损害急性呼吸窘迫综合征患者的气体交换。4. 有证据表明急性呼吸窘迫综合征期间肺血管收缩反应性会发生改变。能够增强肺血管收缩反应性疗效的药物可改善气体交换。如果未来证明安全,环氧合酶抑制剂和阿米三嗪是值得在急性呼吸窘迫综合征中进行测试的有趣化合物。

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