Department of Biology, Fars Science and Research Branch, Islamic Azad University, Fars, Iran.
Department of Biology, Shiraz Branch, Islamic Azad University, Shiraz, Iran.
Sci Rep. 2017 Jun 12;7(1):3221. doi: 10.1038/s41598-017-02748-3.
Brain edema aggravates primary brain injury and increases its mortality rate after ischemic stroke. It is believed that normobaric oxygen therapy (NBO) may produce neuroprotective effects against ischemic stroke; however, reports have been controversial, and its effects on vasogenic brain edema as a major complication of brain ischemia have not been clarified. The present study investigates the effects of NBO on cerebral edema and blood - brain barrier integrity using rat model of ischemic stroke. Transient focal cerebral ischemia was induced in adult male Sprague-Dawley rats by left middle cerebral artery occlusion (MCAO) for 90 min followed by 24 h reperfusion. Early NBO supplementation was started 15 min after MCAO and continued for 90 min. The results of the present study show that early oxygen therapy following acute ischemic stroke does not reduce vasogenic brain edema, nor does it protect against oxidative stress-induced BBB destruction. Additionally, cerebral edema formation occurs in conjunction with an increased mortality rate, serious brain injury, and impairment of brain antioxidant power. These findings suggest that further experimental studies should be carried out to clarify the beneficial effects and potential side effects of early oxygen therapy in acute ischemic stroke before its clinical use.
脑水肿会加重缺血性脑卒中后的原发性脑损伤并增加其死亡率。有研究认为常压氧疗（NBO）可能对缺血性脑卒中具有神经保护作用，但相关报道仍存在争议，其对作为脑缺血主要并发症的血管源性脑水肿的影响尚未阐明。本研究采用大鼠缺血性脑卒中模型，探讨 NBO 对脑水肿和血脑屏障完整性的影响。通过左大脑中动脉闭塞（MCAO）诱导成年雄性 Sprague-Dawley 大鼠短暂性局灶性脑缺血 90 分钟，随后再灌注 24 小时。MCAO 后 15 分钟开始早期补充 NBO，并持续 90 分钟。本研究结果表明，急性缺血性脑卒中后早期氧疗不能减轻血管源性脑水肿，也不能防止氧化应激诱导的 BBB 破坏。此外，脑水肿的形成伴随着死亡率的增加、严重的脑损伤和脑抗氧化能力的损害。这些发现表明，在临床应用之前，应该进行进一步的实验研究，以阐明早期氧疗对急性缺血性脑卒中的有益作用和潜在副作用。
