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Does extracorporeal membrane oxygenation attenuate hypoxic pulmonary vasoconstriction in a porcine model of global alveolar hypoxia?

体外膜肺氧合是否能减弱全肺泡缺氧猪模型中缺氧性肺血管收缩?

  • 影响因子:1.85
  • DOI:10.1111/aas.13588
  • 作者列表:"Holzgraefe B","Larsson A","Eksborg S","Kalzén H
  • 发表时间:2020-03-31
Abstract

BACKGROUND:During severe respiratory failure, hypoxic pulmonary vasoconstriction (HPV) is partly suppressed but may still play a role in increasing pulmonary vascular resistance (PVR). Experimental studies suggest that the degree of HPV during severe respiratory failure is dependent on pulmonary oxygen tension (PvO2 ). Therefore, it has been suggested that increasing PvO2 by veno-venous extracorporeal membrane oxygenation (V-V ECMO) would adequately reduce PVR in V-V ECMO patients. OBJECTIVE:Whether increased PvO2 by V-V ECMO decreases PVR in global alveolar hypoxia. METHODS:Nine landrace pigs were ventilated with a mixture of oxygen and nitrogen. After 15 minutes of stable ventilation and hemodynamics, the animals were cannulated for V-V ECMO. Starting with alveolar normoxia, the fraction of inspiratory oxygen (FI O2 ) was stepwise reduced to establish different degrees of alveolar hypoxia. PvO2 was increased by V-V ECMO. RESULTS:V-V ECMO decreased PVR (from 5.5 [4.5 - 7.1] to 3.4 [2.6 - 3.9] mmHg l-1 min, p=0.006) (median (interquartile range),) during ventilation with FI O2 of 0.15. At lower FI O2 , PVR increased; at FI O2 0.10 to 4.9 [4.2 - 7.0], p=0.036, at FI O2 0.05 to 6.0 [4.3 - 8.6], p=0.002, and at FI O2 0 to 5.4 [3.5 - 7.0] mmHg l-1 min , p=0.05. CONCLUSIONS:The effect of increased PvO2 by V-V ECMO on PVR depended highly on the degree of alveolar hypoxia. Our results partly explain why V-V ECMO does not always reduce right ventricular afterload at severe alveolar hypoxia.

摘要

背景: 在严重呼吸衰竭时,缺氧性肺血管收缩 (HPV) 被部分抑制,但仍可能在增加肺血管阻力 (PVR) 中起作用。实验研究表明,严重呼吸衰竭时 HPV 的程度依赖于肺氧分压 (PvO2)。因此,静脉-静脉体外膜肺氧合 (V-V ECMO) 增加 PvO2 可充分降低 V-V ECMO 患者的 PVR。 目的: V-V ECMO 升高的 PvO2 是否降低全肺泡缺氧时的 PVR。 方法: 9 头长白猪用氧氮混合气通气。15 分钟稳定通气和血流动力学后,动物插管 V-V ECMO。从肺泡常氧开始,逐步降低吸气氧分数 (FI O2),建立不同程度的肺泡缺氧。V-V ECMO 使 PvO2 增加。 结果: V-V ECMO 使 PVR 降低 (从 5.5 [4.5 - 7.1] 降至 3.4 [2.6 - 3.9] mmHg l-1-1 · min,p = 0.006) (中位数 (四分位数间距),) 在 FI O2 为 0.15 的通风过程中。在较低的 FI O2 时,PVR 增加; 在 FI O2 0.10 至 4.9 [4.2 - 7.0] 时,p = 0.036,在 FI O2 0.05 至 6.0 [4.3 - 8.6] 时,p = 0.002,并且在 FI O2 0 到 5.4 [3.5 - 7.0] mmHg l-1 min,p = 0.05。 结论: V-V ECMO 增加 PVR 的 PVR 效应高度依赖于肺泡缺氧程度。我们的结果部分解释了为什么 V-V ECMO 在严重肺泡缺氧时并不总是降低右心室后负荷。

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