{"title":"高氧诱导的全身缺血再灌注损伤继发性呼吸衰竭","authors":"Yu Okuma, Lance B Becker, Tsukasa Yagi, Akane Tanda, Kazumoto Suzuki, Kentaro Shimoda, Goro Kido, Yukihide Kagawa, Koichiro Shinozaki","doi":"10.1007/978-3-031-67458-7_29","DOIUrl":null,"url":null,"abstract":"<p><p>Recent studies revealed that excessive supplemental oxygen, such as inhaled 100% O<sub>2</sub>, 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 (AaDO<sub>2</sub>) 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% O<sub>2</sub> (CA-FiO<sub>2</sub> 1.0) and those with 30% O<sub>2</sub> (CA-FiO<sub>2</sub> 0.3). We prepared a sham surgery group for comparison (sham-FiO<sub>2</sub> 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 AaDO<sub>2</sub>. The lung W/D ratio in the CA-FiO<sub>2</sub> 1.0 group (5.8 ± 0.26) was higher than in the CA-FiO<sub>2</sub> 0.3 (4.6 ± 0.42) and sham-FiO<sub>2</sub> 0.3 groups (4.6 ± 0.38, p < 0.01). There was a significant difference in AaDO<sub>2</sub> between CA-FiO<sub>2</sub> 1.0 (215 ± 49.3) and, CA-FiO<sub>2</sub> 0.3 (36.8 ± 32.3), and sham-FiO<sub>2</sub> 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. AaDO<sub>2</sub> 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 AaDO<sub>2</sub> at a variety level of inhaled O<sub>2</sub>. Given that AaDO<sub>2</sub> measurement is non-invasive, we therefore consider AaDO<sub>2</sub> to be a potentially optimal indicator of post-CA hyperoxic pulmonary injury.</p>","PeriodicalId":7270,"journal":{"name":"Advances in experimental medicine and biology","volume":"1463 ","pages":"173-177"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hyperoxia-Induced Secondary Respiratory Failure in a Systemic Ischaemia-Reperfusion Injury.\",\"authors\":\"Yu Okuma, Lance B Becker, Tsukasa Yagi, Akane Tanda, Kazumoto Suzuki, Kentaro Shimoda, Goro Kido, Yukihide Kagawa, Koichiro Shinozaki\",\"doi\":\"10.1007/978-3-031-67458-7_29\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Recent studies revealed that excessive supplemental oxygen, such as inhaled 100% O<sub>2</sub>, 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 (AaDO<sub>2</sub>) 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% O<sub>2</sub> (CA-FiO<sub>2</sub> 1.0) and those with 30% O<sub>2</sub> (CA-FiO<sub>2</sub> 0.3). We prepared a sham surgery group for comparison (sham-FiO<sub>2</sub> 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 AaDO<sub>2</sub>. The lung W/D ratio in the CA-FiO<sub>2</sub> 1.0 group (5.8 ± 0.26) was higher than in the CA-FiO<sub>2</sub> 0.3 (4.6 ± 0.42) and sham-FiO<sub>2</sub> 0.3 groups (4.6 ± 0.38, p < 0.01). There was a significant difference in AaDO<sub>2</sub> between CA-FiO<sub>2</sub> 1.0 (215 ± 49.3) and, CA-FiO<sub>2</sub> 0.3 (36.8 ± 32.3), and sham-FiO<sub>2</sub> 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. AaDO<sub>2</sub> 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 AaDO<sub>2</sub> at a variety level of inhaled O<sub>2</sub>. Given that AaDO<sub>2</sub> measurement is non-invasive, we therefore consider AaDO<sub>2</sub> to be a potentially optimal indicator of post-CA hyperoxic pulmonary injury.</p>\",\"PeriodicalId\":7270,\"journal\":{\"name\":\"Advances in experimental medicine and biology\",\"volume\":\"1463 \",\"pages\":\"173-177\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in experimental medicine and biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/978-3-031-67458-7_29\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in experimental medicine and biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/978-3-031-67458-7_29","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
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.
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.