高氧诱导的全身缺血再灌注损伤继发性呼吸衰竭

4区 医学 Q2 Biochemistry, Genetics and Molecular Biology
Yu Okuma, Lance B Becker, Tsukasa Yagi, Akane Tanda, Kazumoto Suzuki, Kentaro Shimoda, Goro Kido, Yukihide Kagawa, Koichiro Shinozaki
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引用次数: 0

摘要

最近的研究表明,过量补充氧气(如吸入 100%氧气)会损害心脏骤停(CA)后患者的各种器官功能。因此,补充氧气的最佳指标对于预防高氧器官损伤非常重要。在这项研究中,我们评估了高氧肺损伤,并评估了肺泡-动脉氧差(AaDO2)与肺水肿程度之间的关联。在这项研究中,我们重点研究了高氧诱导的肺损伤及其与脑缺氧后大鼠气体交换参数变化之间的关系。大鼠在窒息 CA 10 分钟后复苏,分为两组:吸入 100%氧气组(CA-FiO2 1.0)和吸入 30%氧气组(CA-FiO2 0.3)。我们还准备了一个假手术组进行比较(sham-FiO2 0.3)。2 小时后,动物被处死,并测量肺干湿(W/D)重量比。我们收集血气结果,测量动脉氧分压与吸入氧分压的比率(p/f 比率),并计算 AaDO2。CA-FiO2 1.0 组的肺 W/D 比值(5.8 ± 0.26)高于 CA-FiO2 0.3 组(4.6 ± 0.42)和假-FiO2 0.3 组(4.6 ± 0.38,CA-FiO2 1.0(215 ± 49.3)、CA-FiO2 0.3(36.8 ± 32.3)和假-FiO2 0.3 组(49.0 ± 20.5,p 2)与 W/D 比率(r = 0.9415,p 2)在各种吸入氧气水平下显示出最强的相关性。鉴于 AaDO2 的测量是非侵入性的,因此我们认为 AaDO2 有可能是判断 CA 后高氧肺损伤的最佳指标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyperoxia-Induced Secondary Respiratory Failure in a Systemic Ischaemia-Reperfusion Injury.

Recent studies revealed that excessive supplemental oxygen, such as inhaled 100% O2, damages various organ functions in post-cardiac arrest (CA) patients. Optimal indicators of supplemental oxygen are therefore important to prevent hyperoxic organ injuries. In this study, we evaluated a hyperoxic pulmonary injury and assessed the association between alveolar-arterial oxygen difference (AaDO2) and a degree of lung oedema. In this study, we focused on the hyperoxia-induced lung injury and its association with changes of gas-exchange parameters in post-CA rats. Rats were resuscitated from 10 min of asphyxial CA and stratified into two groups: those with inhaled 100% O2 (CA-FiO2 1.0) and those with 30% O2 (CA-FiO2 0.3). We prepared a sham surgery group for comparison (sham-FiO2 0.3). After 2 h, animals were sacrificed, and the lung wet-to-dry (W/D) weight ratio was measured. We collected blood gas results and measured the ratio of partial pressure arterial oxygen and fraction of inspired oxygen (p/f ratio), and calculated AaDO2. The lung W/D ratio in the CA-FiO2 1.0 group (5.8 ± 0.26) was higher than in the CA-FiO2 0.3 (4.6 ± 0.42) and sham-FiO2 0.3 groups (4.6 ± 0.38, p < 0.01). There was a significant difference in AaDO2 between CA-FiO2 1.0 (215 ± 49.3) and, CA-FiO2 0.3 (36.8 ± 32.3), and sham-FiO2 0.3 groups (49.0 ± 20.5, p < 0.01). There were also significant changes in pH and blood lactate levels in the early phase among the three groups. AaDO2 showed the strongest correlation with W/D ratio (r = 0.9415, p < 0.0001), followed by pH (r = -0.5131, p = 0.0294) and p/f ratio (r = -0.3861, p = 0.1135). Hyperoxic injury might cause the pulmonary oedema after CA. Measuring respiratory quotient (RQ) in rodents enabled an accurate calculation for AaDO2 at a variety level of inhaled O2. Given that AaDO2 measurement is non-invasive, we therefore consider AaDO2 to be a potentially optimal indicator of post-CA hyperoxic pulmonary injury.

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来源期刊
Advances in experimental medicine and biology
Advances in experimental medicine and biology 医学-医学:研究与实验
CiteScore
5.90
自引率
0.00%
发文量
465
审稿时长
2-4 weeks
期刊介绍: Advances in Experimental Medicine and Biology provides a platform for scientific contributions in the main disciplines of the biomedicine and the life sciences. This series publishes thematic volumes on contemporary research in the areas of microbiology, immunology, neurosciences, biochemistry, biomedical engineering, genetics, physiology, and cancer research. Covering emerging topics and techniques in basic and clinical science, it brings together clinicians and researchers from various fields.
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