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目的 :探讨高压氧对急性脑出血患者神经元特异性烯醇化酶(NSE)、脑源性神经营养因子(BDNF)及细胞间粘附分子-1(sICAM-1)的影响及与脑水肿相关性。方法 :分析2015年1月~2016年6月103例在我院接受治疗的急性脑出血的患者的临床资料,对照组(54例)给予脱水降颅压、营养脑组织,改善脑循环代谢功能,维持酸碱平衡等对症支持治疗。观察组(49例)在对照组的基础上入院3天内给予高压氧治疗。结果 :两组患者接受不同的治疗方案后,观察组患者血清NSE、s ICAM-1水平明显低于对照组,观察组血清BDNF水平明显高于对照组,差异均具有统计学意义;治疗后观察组患者相对脑水肿体积及NIHSS评分水平明显低于对照组;治疗后观察组患者血清NSE及sICAM-1水平与相对脑水肿体积呈正相关,而血清BDNF与相对脑水肿体积呈负相关。结论 :高压氧可明显改善急性脑出血患者脑水肿症状,促进缺损神经功能的恢复,血清NSE、BDNF及sICAM-1的改变可能与脑水肿发病机制存在一定的相关性。
Objective: To investigate the effects of hyperbaric oxygen on neuron-specific enolase (NSE), brain-derived neurotrophic factor (BDNF) and sICAM-1 in patients with acute cerebral hemorrhage and its correlation with cerebral edema Sex. Methods: The clinical data of 103 patients with acute cerebral hemorrhage treated in our hospital from January 2015 to June 2016 were analyzed. The control group (54 cases) was given dehydration and intracranial pressure to nourish brain tissue and improve the metabolic function of cerebral circulation , Maintain acid-base balance and other symptomatic supportive treatment. The observation group (n = 49) received hyperbaric oxygen therapy within 3 days of admission on the basis of the control group. Results: The serum levels of NSE and s ICAM-1 in the observation group were significantly lower than those in the control group after receiving different treatment regimens, the serum levels of BDNF in the observation group were significantly higher than those in the control group, and the differences were statistically significant; after treatment, The relative brain edema volume and the NIHSS score in the group of patients were significantly lower than those in the control group. After treatment, the levels of serum NSE and sICAM-1 in the observation group were positively correlated with the relative volume of brain edema, while the serum BDNF was negatively correlated with the volume of relative brain edema. CONCLUSION: Hyperbaric oxygen can significantly improve the symptoms of cerebral edema in patients with acute cerebral hemorrhage and promote the recovery of neurological deficits. The changes of serum NSE, BDNF and sICAM-1 may be related to the pathogenesis of cerebral edema.