Supplemental oxygen administration during mechanical ventilation reduces diaphragm blood flow and oxygen delivery.
Supplemental oxygen administration during mechanical ventilation reduces diaphragm blood flow and oxygen delivery.
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机械通气期间补充氧气会减少膈肌血流量和氧气输送。
DOI：
10.1152/japplphysiol.00021.2022
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Behnke,BradleyJ
中科院分区：
文献类型：
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作者：
Horn,AndrewG;Kunkel,OliviaN;Schulze,KianaM;Baumfalk,DrydenR;Weber,RamonaE;Poole,DavidC;Behnke,BradleyJ
在机械通气（MV）期间，通常向危重患者给予补充氧气（O2）以对抗低氧血症。以往的研究表明，高氧加重MV诱导的膈肌氧化应激和收缩功能障碍。然而，常氧MV（即21% O2）减少了隔膜灌注和静止隔膜中的O2输送，100% O2 MV的效果尚不清楚。我们测试了一个假设，即MV补充高氧气体（100%O2）将增加膈肌血管阻力，减少动脉血流量和O2输送到更大程度比单独MV。将雌性Sprague-Dawley大鼠（4 - 6月龄）随机分为两组：1）MV ≥ 100%O2，随后MV ≥ 21%O2（n = 9）或2）MV ≥ 21%O2，随后MV ≥ 100%O2（n = 10）。在自主呼吸（SB）、MV ≥ 100%O2和MV ≥ 21%O2期间，通过荧光微球测定膈肌血流量（mL/min/100 g）和血管阻力。与SB组相比，MV ≥ 100%O2和MV ≥ 21%O2组膈肌血管总阻力增加，血流量减少（均P <0.05）。MV ≥ 100%O2组的内侧肋动脉血流量（26 ± 6 mL/min/100 g）低于MV ≥ 21%O2组（51 ± 15 mL/min/100 g; P <0.05）。第二，常氧MV期间加入100%O2加剧了MV诱导的内侧肋膈灌注减少（23 ± 7 vs. 51 ± 15 mL/min/100 g; P <0.05）和O2输送减少（3.4 ± 0.2 vs. 6.4 ± 0.3 mL O2/min/100 g; P <0.05）。这些数据表明，MV期间补充100% O2的管理增加了膈肌血管阻力，并减少灌注和O2输送到一个显着更大的程度比常氧MV。这表明，长时间的MV（即，6小时）与高氧可能会加速MV引起的血管功能障碍，在静止的隔膜和潜在的加剧下游的收缩功能障碍。新&值得注意的是，这是第一项研究，据我们所知，表明，补充氧气（即，100%O2）在机械通气（MV）增强MV引起的减少血管血流量和O2输送。高氧MV加速降低动脉血流量，预计会增强MV诱导的膈肌血管功能障碍，从而增强下游收缩功能障碍。本文提供的数据提供了延长的高氧MV报告的氧化应激和膈肌功能障碍加重的推定机制。
During mechanical ventilation (MV), supplemental oxygen (O2) is commonly administered to critically ill patients to combat hypoxemia. Previous studies demonstrate that hyperoxia exacerbates MV-induced diaphragm oxidative stress and contractile dysfunction. Whereas normoxic MV (ie, 21% O2) diminishes diaphragm perfusion and O2 delivery in the quiescent diaphragm, the effect of MV with 100% O2 is unknown. We tested the hypothesis that MV supplemented with hyperoxic gas (100% O2) would increase diaphragm vascular resistance and reduce diaphragmatic blood flow and O2 delivery to a greater extent than MV alone. Female Sprague–Dawley rats (4–6 mo) were randomly divided into two groups: 1) MV ū 100% O2 followed by MV ū 21% O2 (n= 9) or 2) MV ū 21% O2 followed by MV ū 100% O2 (n= 10). Diaphragmatic blood flow (mL/min/100 g) and vascular resistance were determined, via fluorescent microspheres, during spontaneous breathing (SB), MV ū 100% O2, and MV ū 21% O2. Compared with SB, total diaphragm vascular resistance was increased, and blood flow was decreased with both MV ū 100% O2 and MV ū 21% O2 (all P< 0.05). Medial costal diaphragmatic blood flow was lower with MV ū 100% O2 (26 ą 6 mL/min/100 g) versus MV ū 21% O2 (51 ą 15 mL/min/100 g; P< 0.05). Second, the addition of 100% O2 during normoxic MV exacerbated the MV-induced reductions in medial costal diaphragm perfusion (23 ą 7 vs. 51 ą 15 mL/min/100 g; P< 0.05) and O2 delivery (3.4 ą 0.2 vs. 6.4 ą 0.3 mL O2/min/100 g; P< 0.05). These data demonstrate that administration of supplemental 100% O2 during MV increases diaphragm vascular resistance and diminishes perfusion and O2 delivery to a significantly greater degree than normoxic MV. This suggests that prolonged bouts of MV (ie, 6 h) with hyperoxia may accelerate MV-induced vascular dysfunction in the quiescent diaphragm and potentially exacerbate downstream contractile dysfunction.NEW & NOTEWORTHY This is the first study, to our knowledge, demonstrating that supplemental oxygen (ie, 100% O2) during mechanical ventilation (MV) augments the MV-induced reductions in diaphragmatic blood flow and O2 delivery. The accelerated reduction in diaphragmatic blood flow with hyperoxic MV would be expected to potentiate MV-induced diaphragm vascular dysfunction and consequently, downstream contractile dysfunction. The data presented herein provide a putative mechanism for the exacerbated oxidative stress and diaphragm dysfunction reported with prolonged hyperoxic MV.