Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats
Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats
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DOI：
10.3171/jns.2004.101.3.0499
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发表时间：
2004-09-01
影响因子：
4.1
通讯作者：
Bullock, MR
中科院分区：
文献类型：
--
作者：
Daugherty, WP;Levasseur, JE;Bullock, MR
Object.在本研究中，作者研究了高压氧（HBO）对液压脑损伤后脑组织氧合（PO 2）、氧耗（VO 2）和线粒体功能（氧化还原电位）的影响。脑组织PO 2测定诱导后的侧向液压冲击脑损伤大鼠。高压氧治疗（100%O-2在1.5 ata）显着增加脑组织PO 2在受伤和假受伤的动物。对于VO 2和氧化还原电位实验，使用30%O-2或HBO治疗动物1或4小时（即，4小时30%O-2或1小时HBO和3小时100%O-2）。与接受30%O-2治疗的动物相比，在受伤和假受伤的动物中，经HBO治疗后，VO 2的微量呼吸计测量值显示出显著增加。通过Alamar蓝荧光测量的线粒体氧化还原电位在损伤后1小时表现出损伤诱导的降低。这些减少部分逆转伤后4小时的动物用30%O-2治疗，并完全逆转伤后4小时的动物HBO治疗相比，动物治疗仅1小时。本研究中的数据分析表明，HBO显著增加脑组织损伤后的PO。然而，HBO治疗不足以克服损伤诱导的线粒体氧化还原电位在伤后1小时的下降，但能够恢复氧化还原电位在伤后4小时。此外，HBO诱导增加VO 2，在受伤和假受伤的动物。总之，这些数据表明，线粒体功能受到抑制的损伤和有氧代谢功能的恢复可能会加强与HBO治疗。
Object. In the current study, the authors examined the effects of hyperbaric O-2 (HBO) following fluid-percussion brain injury and its implications on brain tissue oxygenation (PO2) and O-2 consumption (VO2) and mitochondrial function (redox potential).Methods. Cerebral tissue PO2 was measured following induction of a lateral fluid-percussion brain injury in rats. Hyperbaric O-2 treatment (100% O-2 at 1.5 ata) significantly increased brain tissue PO2 in both injured and sham-injured animals. For VO2, and redox potential experiments, animals were treated using 30% O-2 or HBO therapy for 1 or 4 hours (that is, 4 hours 30% O-2 or 1 hour HBO and 3 hours 100% O-2). Microrespirometer measurements of VO2, demonstrated significant increases following HBO treatment in both injured and sham-injured animals when compared with animals that underwent 30% O-2 treatment. Mitochondrial redox potential, as measured by Alamar blue fluorescence, demonstrated injury-induced reductions at 1 hour postinjury. These reductions were partially reversed at 4 hours postinjury in animals treated with 30% O-2, and completely reversed at 4 hours postinjury in animals on HBO therapy when compared with animals treated for only 1 hour.Conclusions. Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO, after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2, in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.