不同程度低血压对双侧颈动脉中度狭窄模型家兔脑损伤的影响
불동정도저혈압대쌍측경동맥중도협착모형가토뇌손상적영향
The effect of hypotension on bilateral carotid artery moderate stenosis in rabbit model brain injury
  • 万方数据
    国际麻醉学与复苏杂志 국제마취학여복소잡지
    International Journal of Anesthesiology and Resuscitation
    2015年 9期 810-814,828 ,共6页

    王春燕%薛朝霞%杨春艳%方爱莉%凡浙录%孟永生%张鹏

    왕춘연%설조하%양춘염%방애리%범절록%맹영생%장붕

    低血压%颈动脉%中度狭窄%S100β%特异性烯醇化酶%海马CA1区%超微结构%脑损伤 低血壓%頸動脈%中度狹窄%S100β%特異性烯醇化酶%海馬CA1區%超微結構%腦損傷
    저혈압%경동맥%중도협착%S100β%특이성희순화매%해마CA1구%초미결구%뇌손상
    Hypotension%Carotid artery%Moderate stenosis%S100β%Neuron-specific enolase%Hippocampal CA1%Ultrastructure%Brain injury
    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(neuron-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30 min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、48 h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48 h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(1 mmHg=0.133 kPa).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.④48 h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(0.468±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＞0.4 μg/L和NSE含量＞17.0 μg/L作为早期脑损伤的临界指标.
    목적 통과관찰불동정도저혈압대쌍측경동맥중도협착모형가토혈청S100β단백화신경원특이성희순화매(neuron-specific enolase,NSE)적표체급해마CA1구신경원초미결구적영향,탐토저혈압여뇌손상적관계. 방법 채용완전수궤분조방법장30지신서란가토분위6조(매조5지):공백대조조(E조)불주임하처리,기여25지제비성쌍측경동맥중도협착모형;병박분1조(B1조)화초산감유1조(A1조)강저기기출혈압적10％～15％,병박분2조(B2조)화초산감유2조(A2조)강저기기출혈압적15％～20％,각조강압유지30 min후회복기출혈압;단순협착조(D조)불주강압처리.류취회복혈압후12、24、48 h혈액,매련면역흡부법(enzyme-linked immunosorbent assay,ELISA)검측혈청S100β화NSE;재회복혈압48 h후,단두취뇌,투사전자현미경(전경)관찰해마CA1구신경원적초미결구. 결과 ①가토평균동맥압(mean arterial pressure,MAP)위(120.1±3.7) mmHg(1 mmHg=0.133 kPa).②각시간점각조(제E조외)여D조비교,S100β화NSE적표체증고(P＜0.05);A2조여A1조、B2조여B1조비교,각시간점S100β화NSE적표체증고(P＜0.05);초산감유조여병박분조비교,각시간점S100β화NSE적표체증고(P＜0.05).③전경발현:E조、D조신경원세포핵막청석,핵인완정,포질내세포기결구완정.A1조화B1조신경원세포핵막경미추축,포질내세포기미견명현이상;B2조신경원세포핵막추축명현,포질내세포기배렬문란,선립체수종정타원형;A2조신경원세포핵막추축엄중,포질내세포기감소,선립체수종정원형.④48 h시,여E조、D조、A1조、B1조비교,A2조、B2조가토해마CA1구신경원세포출현료조기뇌손상개변,차시A2조S100β농도위(0.468±0.021) μg/L、NSE농도위(18.51±0.85) μg/L,B2조S100β농도위(0.423±0.015)g/L、NSE농도위(17.42±0.23) μg/L(P＜0.05). 결론 쌍측경동맥중도협착모형가토혈압하강10％～15％시,혈청S100β화NSE함량균증고,단가토미출현조기뇌손상;혈압하강15％～20％시,불부혈청S100β화NSE함량균증고,동시가토발생조기뇌손상.추천장혈청S100β함량＞0.4 μg/L화NSE함량＞17.0 μg/L작위조기뇌손상적림계지표.
    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 neuronspecific enolase (NSE) and the expression of S100α 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 B1) 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 ultrastructure 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) was significant (P＜0.05).Compared with A1,the expressions of S100β and NSE in A2 were significantly different (P＜0.05).Compared with B1,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,B 1 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 S 100β 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＞0.4 μg/L and NSE＞17.0 μg/L as a critical indicator of early brain injury.
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