Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Crit Care Med. 2021 Sep 1;49(9):e891-e901. doi: 10.1097/CCM.0000000000005057.
To investigate if oxygen could unload the right ventricle and improve right ventricle function in a porcine model mimicking intermediate-high risk acute pulmonary embolism.
Controlled, blinded, animal study.
Tertiary university hospital, animal research laboratory.
Female, Danish pigs (n = 16, approximately 60 kg).
Acute autologous pulmonary embolism was induced until doubling of baseline mean pulmonary arterial pressure. Group 1 animals (n = 8) received increasing Fio2 (40%, 60%, and 100%) for time intervals of 15 minutes returning to atmospheric air between each level of Fio2. In group 2 (n = 8), the effects of Fio2 40% maintained over 75 minutes were studied. In both groups, pulmonary vasodilatation from inhaled nitric oxide (40 parts per million) was used as a positive control.
Effects were evaluated by biventricular pressure-volume loop recordings, right heart catheterization, and arterial and mixed venous blood gasses. Pulmonary embolism increased mean pulmonary arterial pressure from 15 ± 4 to 33 ± 6 mm Hg (p = 0.0002) and caused right ventricle dysfunction (p < 0.05) with troponin release (p < 0.0001). In group 1, increasing Fio2 lowered mean pulmonary arterial pressure (p < 0.0001) and pulmonary vascular resistance (p = 0.0056) and decreased right ventricle volumes (p = 0.0018) and right ventricle mechanical work (p = 0.034). Oxygenation was improved and pulmonary shunt was lowered (p < 0.0001). Maximal hemodynamic effects were seen at Fio2 40% with no additional benefit from higher fractions of oxygen. In group 2, the effects of Fio2 40% were persistent over 75 minutes. Supplemental oxygen showed the same pulmonary vasodilator efficacy as inhaled nitric oxide (40 parts per million). No adverse effects were observed.
In a porcine model mimicking intermediate-high risk pulmonary embolism, oxygen therapy reduced right ventricle afterload and lowered right ventricle mechanical work. The effects were immediately present and persistent and were similar to inhaled nitric oxide. The intervention is easy and safe. The study motivates extended clinical evaluation of supplemental oxygen in acute pulmonary embolism.
在模拟中高危急性肺栓塞的猪模型中，研究氧是否可以减轻右心室负担并改善右心室功能。
对照、盲法、动物研究。
三级大学医院，动物研究实验室。
雌性丹麦猪（n=16，约 60kg）。
急性自体肺栓塞直至基础平均肺动脉压增加一倍。第 1 组动物（n=8）接受 15 分钟的递增 Fio2（40%、60%和 100%），然后在每个 Fio2 水平之间返回大气空气。第 2 组（n=8）研究了 Fio2 40%持续 75 分钟的效果。在两组中，吸入一氧化氮（40ppm）的肺血管舒张作用被用作阳性对照。
通过双心室压力-容积环记录、右心导管检查以及动脉和混合静脉血气来评估效果。肺栓塞使平均肺动脉压从 15±4 增加到 33±6mmHg（p=0.0002），并导致右心室功能障碍（p<0.05），肌钙蛋白释放（p<0.0001）。在第 1 组中，增加 Fio2 降低了平均肺动脉压（p<0.0001）和肺血管阻力（p=0.0056），降低了右心室容积（p=0.0018）和右心室机械功（p=0.034）。氧合作用得到改善，肺分流减少（p<0.0001）。在 Fio2 40%时观察到最大的血流动力学效果，而更高的氧气分数没有额外的益处。在第 2 组中，Fio2 40%的作用持续 75 分钟。补充氧气显示出与吸入一氧化氮（40ppm）相同的肺血管舒张作用。未观察到不良反应。
在模拟中高危肺栓塞的猪模型中，氧疗可减轻右心室后负荷并降低右心室机械功。效果立即出现并持续存在，与吸入一氧化氮相似。该干预措施简单安全。该研究激发了对急性肺栓塞中补充氧气的扩展临床评估。
