TY - CHAP
T1 - Hyperoxia-Induced Secondary Respiratory Failure in a Systemic Ischaemia-Reperfusion Injury
AU - Okuma, Yu
AU - Becker, Lance B.
AU - Yagi, Tsukasa
AU - Tanda, Akane
AU - Suzuki, Kazumoto
AU - Shimoda, Kentaro
AU - Kido, Goro
AU - Kagawa, Yukihide
AU - Shinozaki, Koichiro
N1 - Publisher Copyright:
© Oxygen Transport to Tissue International 2024.
PY - 2024
Y1 - 2024
N2 - 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.
AB - 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.
KW - Alveolar-arterial oxygen difference (AaDO)
KW - Hyperoxia
KW - Ischemia-reperfusion injury
KW - Respiratory quotient (RQ)
KW - Secondary respiratory failure
UR - http://www.scopus.com/inward/record.url?scp=85206275359&partnerID=8YFLogxK
U2 - 10.1007/978-3-031-67458-7_29
DO - 10.1007/978-3-031-67458-7_29
M3 - Chapter
C2 - 39400819
AN - SCOPUS:85206275359
T3 - Advances in Experimental Medicine and Biology
SP - 173
EP - 177
BT - Advances in Experimental Medicine and Biology
PB - Springer
ER -