右美托咪定对脑膜瘤患者术后血浆中脑源性神经生长因子水平的影响

目的 探讨右美托咪定对脑膜瘤患者术后血浆中脑源性神经生长因子(Brain-derived neurotrophic factor,BDNF)水平的影响。方法 选择2017年7月-2019年6月120例脑膜瘤患者展开研究,将患者随机分为对照(生理盐水)组和右美(右美托咪定)组,每组各60例; 记录2组患者拔管时间,比较2组患者拔管10 min后(T3)、拔管1 h后(T4)、拔管6 h后(T5)、拔管12 h后(T6)的平均动脉压(Mean arterial pressure,MAP)、血氧饱和度(Oxyhemoglobin saturation,SPO₂)、心率(Heart rate,HR)、呼吸频率、Ramsay评分、格拉斯哥昏迷量表(Glasgow coma scale,GCS)评分、拔管即刻(T2)至拔管12 h后(T6)内躁动发生率; 观察2组患者插管20 min后(T1),T3,T4,T5,T6 BDNF水平变化,利用简易精神状态量表(Mini-Mental state examination,MMSE)评分和蒙特利尔认知量表(Montreal cognitive scale,MoCA)评分评估2组患者术前(T0)、拔管24 h后(T7)、拔管48 h后(T8)、拔管3 d后(T9)、拔管7 d后(T10)、拔管1个月后(T11)的认知功能变化。结果 右美组拔管时间明显长于对照组(P<0.05); 右美组T3,T4,T5,T6 MAP,HR明显低于对照组(P<0.05),Ramsay评分、GCS评分明显高于对照组(P<0.05),2组患者SPO₂、呼吸频率比较无明显差异(P>0.05); 右美组的T2躁动发生率20.00%与对照组的26.67%比较无明显差异(P>0.05),T6躁动发生率为8.33%,明显低于对照组的18.33%(P<0.05)。与T1比较,2组患者T4,T5 BDNF水平明显升高(P<0.05),且右美组患者T6 BDNF水平同样明显升高(P<0.05),对照组患者T6 BDNF水平未发生明显变化(P>0.05); 右美组T6 BDNF水平明显高于对照组(P<0.05)。与T0比较,对照组患者T7-T11 MMSE评分、MOCA评分下降(P<0.05),右美组患者T7-T9 MMSE评分、MOCA评分下降(P<0.05),T10,T11 MMSE评分、MOCA评分上升(P<0.05); 右美组T10,T11 MMSE评分、MOCA评分均高于对照组(P<0.05)。结论 右美托咪定具有显著的镇静效果,能显著改善患者的认知功能,其机制可能是通过上调BDNF表达来对患者发挥脑保护作用。

The effects of dexmedetomidine on plasma brain-derived nerve growth factor levels in patients with meningioma after surgery

ObjectiveTo investigate the effects of dexmedetomidine on plasma brain-derived nerve growth factor(BDNF)levels in patients with meningioma after surgery.Methods From July 2017 to June 2019, 120 postoperative patients in department of craniocerebral surgery were selected for the study, and the patients were randomly divided into two groups: control group(normal saline)and dexmedetomidine group(dexmedetomidine), with 60 cases in each group. The extubation time of the two groups was recorded, and the mean arterial pressure(MAP), blood oxygen saturation(SPO₂), heart rate(HR), respiratory rate, Ramsay score, Glasgow coma score(GCS)and at 10 min(T3), 1 h(T4), 6 h(T5)and 12 h(T6)after extubation were compared between the two groups, and the incidence of agitation from immediately(T2)to 12 h(T6)after extubation, and the changes of BDNF were counted in the two groups at 20min after intubation(T1)and at T3, T4, T5 and T6, and the Mini-Mental State Examination(MMSE)score and the Montreal Cognitive Assessment Scale(MOCA)score were used to evaluate the cognitive function changes in the two groups at preoperative(T0), at 24 h(T7), 48 h(T8), 3 d(T9), 7 d(T10)and 1 month(T11)after extubation.Results The extubation time in the dexmedetomidine group was significantly longer than that in the control group(P<0.05). The MAP, HR at T3, T4, T5 and T6 in the dexmedetomidine group were significantly lower than those in the control group(P<0.05)while the Ramsay score and GCS score were significantly higher than those in the control group(P<0.05), and there were no significant differences in the SPO₂ and respiratory rate between the two groups(P>0.05). There was no significant difference in the incidence rate of agitation at T2 between dexmedetomidine group and control group(20.00% vs 26.67%)(P>0.05). The incidence of agitation at T6 was significantly lower than that in the control group(8.33% vs 18.33%)(P<0.05). Compared with at T1, the BDNF levels in the two groups were increased significantly at T4 and T5(P<0.05), and the BDNF levels at T6 in the dexmedetomidine group was also increased significantly(P<0.05), and the BDNF levels at T6 in the control group did not change significantly(P>0.05). The BDNF levels at T6 in dexmedetomidine group were significantly higher than that in the control group(P<0.05). Compared with at T0, the MMSE score and MOCA score in the control group were decreased at T7-T11(P<0.05), and the MMSE score and MOCA score in the dexmedetomidine group were decreased at T7-T9(P<0.05), and the MMSE score and MOCA score were increased at T10,T11(P<0.05), and the MMSE score and MOCA score at T10 and T11 in the dexmedetomidine group were higher than those in the control group(P<0.05).Conclusion Dexmedetomidine has a significant sedative effect after craniotomy and can significantly improve the cognitive function. It may play a protective role in sedative patients after craniotomy through up-regulating the expression of BDNF.