Abstract
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.
Highlights
Brain edema is a life-threatening complication of cerebral infarction, which aggravates ischemic brain injury by compression of the cerebral vasculature and reduction of blood flow to the penumbral region[1]
Ischemia increased the neurological deficit score (NDS) of ischemic rats in the control group compared with sham animals (P < 0.001), and early oxygen therapy did not produce any improvement in neurological function (Fig. 1C)
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 blood-brain barrier (BBB) destruction in adult male Sprague-Dawley rats
Summary
Brain edema is a life-threatening complication of cerebral infarction, which aggravates ischemic brain injury by compression of the cerebral vasculature and reduction of blood flow to the penumbral region[1]. Vasogenic edema is characterized by increased extracellular fluid volume due to destruction of the blood-brain barrier (BBB)[2]. This type of edema develops within the first few hours to days after a stroke. Transient brain ischemia and subsequent reperfusion enhances the production of oxygen free radicals and lipid peroxidation as one of the main causes of BBB destruction and subsequent vasogenic cerebral edema[3, 4]. Due to the profound controversy surrounding oxygen therapy in acute ischemic stroke and limited availability of data about its effects on brain edema as a major complication of brain ischemia, in this study, we evaluated the effects of short and early oxygen therapy on ischemic brain injury and behavioral outcome at the first step. We assessed the effects of oxygen therapy on vasogenic brain edema, and we quantified BBB damage as a result of lipid peroxidation and brain antioxidant capacity with FRAP assay
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