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Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage

机译:高压氧合对实验性蛛网膜下腔出血后脑皮质膜Na+、K+-ATP酶及膜流动性的影响

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摘要

It is reported that CNS hemorrage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K+-ATPase activity measurement, and spin-label studies were performed on crude synpatosomal membranes. Subarachnoid hemorrhage decreased Na+, K+-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.
机译:据报道,中枢神经系统出血会导致膜功能障碍,并可能因继发性缺血或缺氧而加剧这种损伤。由于高压氧可以改善氧代谢,因此可以减少这种膜损伤。本研究旨在揭示高压氧合是否影响出血后的膜改变。蛛网膜下腔出血诱导后30分钟,大鼠用高压氧合2 ATA治疗1小时。大鼠在蛛网膜下腔出血诱导后2小时被斩首。对粗突突体膜进行Na+、K+-ATPase活性测量和自旋标记研究。蛛网膜下腔出血降低Na+、K+-ATP酶活性。自旋标记研究表明,蛛网膜下腔出血后,膜表面附近的疏水部分变得更加坚硬,膜蛋白标记的巯基的迁移率降低。高压氧治疗显著改善了大部分蛛网膜下腔出血引起的改变。我们得出结论,高压氧合可能是急性蛛网膜下腔出血的有益治疗方法。

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