*Department of Disaster and Emergency Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan †Department of Anaesthesia, Nishiwaki Municipal Hospital, Nishiwaki, Hyogo, Japan ‡Department of Pharmacy, Tokushima University Hospital, Tokushima, Japan §Department of Pharmacology, Osaka City University Graduate School of Medicine, Osaka, Japan ||Department of Pathology and Host Defense, Kagawa University, Kitagun, Kagawa, Japan ¶Department of Anaesthesia, Higashiosaka City Medical Center, Higashiosaka, Japan.
Shock. 2017 Nov;48(5):590-594. doi: 10.1097/SHK.0000000000000891.
After hypoxia, reoxygenation with air is the consensus treatment for full-term neonates; however, the effect of hyperoxic reoxygenation of adults is unknown. The present study was designed to investigate the effects of reoxygenation with 100% oxygen after hypoxia on inflammation and apoptosis in mice. Eight-week-old mice were either subjected to hypoxia in 8% oxygen for 30 min or air served as controls. Following hypoxia, mice underwent reoxygenation for 30 min with 21% or 100% oxygen. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), caspase-3 and brain derived neurotrophic factor (BDNF) mRNA study and histopathological study were performed. Reoxygenation with 100% oxygen significantly increased TNF-α (2.5 h after hypoxia), IL-1β (5 h after hypoxia), caspase-3 (8 h after hypoxia) mRNA levels in the whole brain compared with 21% oxygen, and significantly decreased erythropoietin mRNA expression compared with 21% oxygen 9 h after reoxygenation. However, reoxygenation with 100% oxygen and 21% oxygen significantly decreased BDNF mRNA levels compared with control air group. There were no clear abnormal findings showing neuronal death among the three groups. Reoxygenation with 100% oxygen after hypoxia induced inflammation and apoptosis in adult mice. Therefore, these results suggest that the reoxygenation with 100% oxygen after hypoxia has harmful effects on adult brain as well as on neonatal brain.
缺氧后，用空气进行再氧化是足月新生儿的共识治疗方法；然而，成人用高浓度氧气进行再氧化的效果尚不清楚。本研究旨在探讨缺氧后用 100%氧气进行再氧化对小鼠炎症和细胞凋亡的影响。将 8 周大的小鼠置于 8%氧气中缺氧 30 分钟，或作为对照用空气处理。缺氧后，小鼠用 21%或 100%氧气进行 30 分钟的再氧化。进行肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、半胱天冬酶-3 和脑源性神经营养因子（BDNF）mRNA 研究和组织病理学研究。与 21%氧气相比，100%氧气再氧化显著增加了整个大脑中的 TNF-α（缺氧后 2.5 小时）、IL-1β（缺氧后 5 小时）和 caspase-3（缺氧后 8 小时）mRNA 水平，并且与 21%氧气相比，在再氧化后 9 小时显著降低了促红细胞生成素 mRNA 表达。然而，与空气对照组相比，100%氧气和 21%氧气再氧化均显著降低了 BDNF mRNA 水平。三组之间没有明显的异常发现表明神经元死亡。缺氧后用 100%氧气进行再氧化在成年小鼠中诱导了炎症和细胞凋亡。因此，这些结果表明，缺氧后用 100%氧气进行再氧化对成人脑和新生儿脑都有有害影响。
