中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (9): 1445-1449.doi: 10.4103/1673-5374.191218

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

高压氧治疗亚急性颅脑损伤的神经保护作用：不是即刻提高脑氧饱和度和氧分压实现的

  

  • 收稿日期:2016-08-20 出版日期:2016-09-30 发布日期:2016-09-30
  • 基金资助:
    苏州重大医学项目(Szxk201504)

Neuroprotection of hyperbaric oxygen therapy in sub-acute traumatic brain injury: not by immediately improving cerebral oxygen saturation and oxygen partial pressure

Bao-chun Zhou1, Li-jun Liu1, *, Bing Liu2   

  1. 1 Department of Emergency and Intensive Care Unit, the Second Affliated Hospital of Soochow University, Suzhou, Jiangsu Province, China 2 Department of Neurosurgery, High-tech District Branch of the Second Affliated Hospital of Soochow University, Suzhou, Jiangsu Province, China
  • Received:2016-08-20 Online:2016-09-30 Published:2016-09-30
  • Contact: Li-jun Liu, Ph.D., lijunliusz@sina.com.
  • Supported by:
    This study was supported by a grant from Suzhou Key Medicine Project Fund of China, No. Szxk201504.

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摘要：

高压氧治疗可促进颅脑创伤患者的神经功能恢复，但具体神经保护机制尚不清楚。我们假设亚急性颅脑损伤患者经高压氧治疗后，脑组织氧分压和血氧饱和度升高而发挥的神经保护作用。试验将40例亚急性颅脑损伤患者接受90 min 100%氧浓度的高压氧治疗。在接受高压氧治疗前后30 min，采用INVOS5100脑氧饱和度监测仪监测颅脑损伤患者脑氧饱和度变化。健康志愿者20例仅监测脑氧饱和度和氧分压，不进行高压氧治疗。结果发现，亚急性颅脑损伤患者接受90 min，100%氧浓度的高压氧治疗。结果发现，亚急性脑损伤患者在高压氧治疗前30 min和治疗后30 min，脑氧饱和度无明显变化，但均明显低于健康志愿者。高压氧治疗后30 min脑损伤患者的氧分压还较治疗前显著降低。说明高压氧治疗亚急性颅脑损伤患者的机制不是通过即刻提高脑氧饱和度和氧分压实现的，具体机制需进一步探讨。 

orcid: 0000-0001-6031-101X (Li-jun Liu)

关键词: 神经再生, 高压氧, 近红外光谱, 脑氧饱和度, 创伤性脑损伤, 氧分压, 氧代谢, 创伤修复, 神经功能, 血气分析, 机制

Abstract: Although hyperbaric oxygen (HBO) therapy can promote the recovery of neural function in patients who have suffered traumatic brain injury (TBI), the underlying mechanism is unclear. We hypothesized that hyperbaric oxygen treatment plays a neuroprotective role in TBI by increasing regional transcranial oxygen saturation (rSO2) and oxygen partial pressure (PaO2). To test this idea, we compared two groups: a control group with 20 healthy people and a treatment group with 40 TBI patients. The 40 patients were given 100% oxygen of HBO for 90 minutes. Changes in rSO2 were measured. The controls were also examined for rSO2 and PaO2, but received no treatment. rSO2 levels in the patients did not differ signifcantly after treatment, but levels before and after treatment were signifcantly lower than those in the control group. PaO2 levels were signifcantly decreased after the 30-minute HBO treatment. Our fndings suggest that there is a disorder of oxygen metabolism in patients with sub-acute TBI. HBO does not immediately affect cerebral oxygen metabolism, and the underlying mechanism still needs to be studied in depth.

Key words: nerve regeneration, hyperbaric oxygen, near-infrared spectroscopy, cerebral oxygen saturation, traumatic brain injury, oxygen partial pressure, oxygen metabolism, wound healing, neurological function, blood gas analysis, neural regeneration