摘要
目的通过观察不同程度低血压对双侧颈动脉中度狭窄模型家兔血清S100β蛋白和神经元特异性烯醇化酶（neumn-specific enolase，NSE）的表达及海马CA1区神经元超微结构的影响，探讨低血压与脑损伤的关系。方法采用完全随机分组方法将30只新西兰家兔分为6组（每组5只）：空白对照组（E组）不做任何处理，其余25只制备成双侧颈动脉中度狭窄模型；丙泊酚1组（B1组）和硝酸甘油1组（A1组）降低其基础血压的10％-15％，丙泊酚2组（B2组）和硝酸甘油2组（A2组）降低其基础血压的15％。20％，各组降压维持30min后恢复基础血压；单纯狭窄组（D组）不做降压处理。留取恢复血压后12、24、48h血液，酶联免疫吸附法（enzyme-linked immunosorbent assay，ELISA）检测血清S100β和NSE；在恢复血压48h后，断头取脑，透射电子显微镜（电镜）观察海马CA1区神经元的超微结构。结果①家兔平均动脉压（mean arterial pressure，MAP）为（120．1±3．7）mmHg（1mmHg=0．133kPa）。②各时间点各组（除E组外）与D组比较，S100β和NSE的表达增高（P〈0．05）；A2组与A1组、B2组与B1组比较，各时间点S100β和NSE的表达增高（P〈0．05）；硝酸甘油组与丙泊酚组比较，各时间点S100β和NSE的表达增高（P〈0．05）。③电镜发现：E组、D组神经元细胞核膜清晰，核仁完整，胞质内细胞器结构完整。A1组和B1组神经元细胞核膜轻微皱缩，胞质内细胞器未见明显异常；B2组神经元细胞核膜皱缩明显，胞质内细胞器排列紊乱，线粒体水肿呈椭圆形；A2组神经元细胞核膜皱缩严重，胞质内细胞器减少，线粒体水肿呈圆形。④48h时，与E组、D组、A1组、B1组比较，A2组、B2组家兔海马CA1区神经元细胞出现了早期脑损伤改变，此时A2组S100β浓度为（O．468±0．021）μg／L、NSE浓度为（18．51±0．85）μg／L，B2组S100β浓度为（0．423±0．015）g/L、NSE浓度为（17．42±0．23）μg／L（P〈0．05）。结论双侧颈动脉中度狭窄模型家兔血压下降10％，15％时，血清S100β和NSE含量均增高，但家兔未出现早期脑损伤；血压下降15％～20％时，不仅血清S100β和NSE含量均增高，同时家兔发生早期脑损伤。推荐将血清S100β含量〉0．4μg/L和NSE含量〉17．0μg／L作为早期脑损伤的临界指标。
Objective In order to explore the relationship between hypotension and brain tissue damage, we observed the effect of different levels of hypotension on the carotid artery moderate stenosis rabbit model plasma neuron-specific enolase neuron- specific enolase （NSE） and the expression of S100β and the ultrastructure of hippocampus CA1. Methods Thirty rabbits were equally and randomly divided into 6 groups （n=5）. The normal group （group E ） was not processed. The rest 5 groups were made into models with bilateral carotid moderate stenosis. Propofol group 1（group B 1 ） and nitroglocerin group 1 （group A1 ） were reduced by 10%-15%, 15%-20% of basal blood pressure. Propofol group 2（group B2 ） and nitroglocerin group（group B2 ） were reduced by 10%-15%, 15%-20% of basal blood pressure, 30 min later, all groups were restored to basal blood pressure. Control group （group D）was not processed. Blood specimens were taken at 12, 24 h and 48 h respectively after blood pressure recovered. S100β and NSE were measured by enzyme-linked immunosorbent assay （ELISA）. 48 h after blood pressure was restored, the uhrastructure of hippocampus CA1 was observed by electron microscope. Results （1） The mean arterial pressure（MAP） of rabbit is（120.1±3.7） mmHg （ 1 mmHg= 0.133 kPa）. （2） Compared with group D, the difference of the expressions of S100β and NSE of each group （besides group E） wassignificant （P〈O.05）. Compared with A1, the expressions of S100β and NSE in A2 were significantly different （P〈0.05）. Compared with BI, the expressions of S100β and NSE in B2 were significantly different （P〈0.05）. （3） Through the electron microscope, it was found that neural cells of group E and group D have clear nuclear membrane, complete nucleolus and organelles structure in the endochylema. In group A1 and group B1, nuclear membranes shrank slightly, while organelles in the endochylema had no apparent abnormal sign. In group B2 nuclear membranes shrank distinctly, organelles in the endochylema had a disordered arrangement, mitochondria edema was elliptical, in group A2, nuclear membranes shrank severely, the number of organelles in the endochylema decreased, mitochodria edema was round. （4） At the time of 48 h, compared with the E, D, A1, B1 group, A2, B2 rabbits hippocampal CA1 neurons appeared early brain injury changes, A2 group plasma S100β concentration was （0.468±0.021） μg/L, NSE concentration was（ 18.51±0.85 ） μg/L, B2 group plasma S100β concentration was（0.423±0.015） μg/L, NSE concentration was （17.42±0.23） μg/L. Conclusions When basal blood pressure reduced 10%-15%, the carotid artery moderate stenosis rabbit model had an increase in the expression of S100β and NES without brain tissue damage. When reduced 15%-20%, brain tissue would be early damaged. And recommended that the plasma S100β〉0.4μg/L and NSE〉17.0 μg/L as a critical indicator of early brain injury.
出处
《国际麻醉学与复苏杂志》
CAS
2015年第9期810-814,828,共6页
International Journal of Anesthesiology and Resuscitation
