中华生物医学工程杂志
中華生物醫學工程雜誌
중화생물의학공정잡지
CHINESE JOURNAL OF BIOMEDICAL ENGINEERING
2008年
4期
274-277
,共4页
脑缺血%再灌注损伤%亚低温%钙离子拮抗剂%神经元特异性烯醇化酶%颈静脉血氧饱和度%脑水肿
腦缺血%再灌註損傷%亞低溫%鈣離子拮抗劑%神經元特異性烯醇化酶%頸靜脈血氧飽和度%腦水腫
뇌결혈%재관주손상%아저온%개리자길항제%신경원특이성희순화매%경정맥혈양포화도%뇌수종
Cerebral ischemic%Reperfusion injury%Sub-hypothermia%Calcium antagonist%Neurons specific enolase%Saturation of jugular vein oxygen%Brain edema
目的 探讨亚低温及尼莫地平对脑缺血再灌注损伤的保护作用及机制.方法 健康新西兰大耳白兔24只,随机分为健康对照组(Ⅰ组)、常温缺血再灌注损伤组(Ⅱ组)、亚低温缺血再灌注损伤组(Ⅲ组)、亚低温+尼萸地平组(Ⅳ组),每组6只.采用双侧颈总动脉夹闭低血压脑缺血模型,除健康对照组外,各组均行脑缺血30 min,再灌注3 h;Ⅲ组在双侧颈总动脉夹闭的同时行局部脑组织亚低温处理,Ⅳ组在夹闭的同时行局部脑组织亚低温+尼萸地平10μg·kg-1·h-1静脉输注并维持至再灌注后3 h.常规监测鼓膜温度、创伤性平均动脉压(MAP)和中心静脉压(CVP).分别于缺血前、缺血30 min、再灌注30、60、120、180 min采血标本,血气分析仪检测颈静脉血氧饱和度(SjvO2).再灌注3 h后处死动物,取脑称干湿重比计算脑含水量.ELISA方法检测血清烯醇化酶(NSE)含量.结果 脑含水量Ⅱ组>Ⅲ组>Ⅳ组.Ⅱ组全脑缺血冉灌注后60 min,血清NSE含量明显升高至(14.07±0.67)μg/L,120 min达高峰(18.53±0.85)μg/L,而SjvO2降低至(66±7.6)%.Ⅲ组冉灌注60min时血清NSE含量下降至(7.27±0.25)μg/L;180 min时至(9.17±0.57)μg/L,SjvO2升高至(91±4.5)%,与Ⅱ组比较差异有统计学意义(P均<0.01).Ⅳ组的血清NSE含量显著低于Ⅲ组,差异具有统计学意义.再灌注30 min,颈静脉血氧饱和度升高,Ⅲ组与Ⅳ组差异无统计学意义(P>0.05).结论 局部脑组织亚低温联合尼莫地平静脉输注能显著减少兔全脑缺血再灌注后血清NSE表达,升高SjvO2,减轻缺血再灌注损伤所致的脑水肿.
目的 探討亞低溫及尼莫地平對腦缺血再灌註損傷的保護作用及機製.方法 健康新西蘭大耳白兔24隻,隨機分為健康對照組(Ⅰ組)、常溫缺血再灌註損傷組(Ⅱ組)、亞低溫缺血再灌註損傷組(Ⅲ組)、亞低溫+尼萸地平組(Ⅳ組),每組6隻.採用雙側頸總動脈夾閉低血壓腦缺血模型,除健康對照組外,各組均行腦缺血30 min,再灌註3 h;Ⅲ組在雙側頸總動脈夾閉的同時行跼部腦組織亞低溫處理,Ⅳ組在夾閉的同時行跼部腦組織亞低溫+尼萸地平10μg·kg-1·h-1靜脈輸註併維持至再灌註後3 h.常規鑑測鼓膜溫度、創傷性平均動脈壓(MAP)和中心靜脈壓(CVP).分彆于缺血前、缺血30 min、再灌註30、60、120、180 min採血標本,血氣分析儀檢測頸靜脈血氧飽和度(SjvO2).再灌註3 h後處死動物,取腦稱榦濕重比計算腦含水量.ELISA方法檢測血清烯醇化酶(NSE)含量.結果 腦含水量Ⅱ組>Ⅲ組>Ⅳ組.Ⅱ組全腦缺血冉灌註後60 min,血清NSE含量明顯升高至(14.07±0.67)μg/L,120 min達高峰(18.53±0.85)μg/L,而SjvO2降低至(66±7.6)%.Ⅲ組冉灌註60min時血清NSE含量下降至(7.27±0.25)μg/L;180 min時至(9.17±0.57)μg/L,SjvO2升高至(91±4.5)%,與Ⅱ組比較差異有統計學意義(P均<0.01).Ⅳ組的血清NSE含量顯著低于Ⅲ組,差異具有統計學意義.再灌註30 min,頸靜脈血氧飽和度升高,Ⅲ組與Ⅳ組差異無統計學意義(P>0.05).結論 跼部腦組織亞低溫聯閤尼莫地平靜脈輸註能顯著減少兔全腦缺血再灌註後血清NSE錶達,升高SjvO2,減輕缺血再灌註損傷所緻的腦水腫.
목적 탐토아저온급니막지평대뇌결혈재관주손상적보호작용급궤제.방법 건강신서란대이백토24지,수궤분위건강대조조(Ⅰ조)、상온결혈재관주손상조(Ⅱ조)、아저온결혈재관주손상조(Ⅲ조)、아저온+니유지평조(Ⅳ조),매조6지.채용쌍측경총동맥협폐저혈압뇌결혈모형,제건강대조조외,각조균행뇌결혈30 min,재관주3 h;Ⅲ조재쌍측경총동맥협폐적동시행국부뇌조직아저온처리,Ⅳ조재협폐적동시행국부뇌조직아저온+니유지평10μg·kg-1·h-1정맥수주병유지지재관주후3 h.상규감측고막온도、창상성평균동맥압(MAP)화중심정맥압(CVP).분별우결혈전、결혈30 min、재관주30、60、120、180 min채혈표본,혈기분석의검측경정맥혈양포화도(SjvO2).재관주3 h후처사동물,취뇌칭간습중비계산뇌함수량.ELISA방법검측혈청희순화매(NSE)함량.결과 뇌함수량Ⅱ조>Ⅲ조>Ⅳ조.Ⅱ조전뇌결혈염관주후60 min,혈청NSE함량명현승고지(14.07±0.67)μg/L,120 min체고봉(18.53±0.85)μg/L,이SjvO2강저지(66±7.6)%.Ⅲ조염관주60min시혈청NSE함량하강지(7.27±0.25)μg/L;180 min시지(9.17±0.57)μg/L,SjvO2승고지(91±4.5)%,여Ⅱ조비교차이유통계학의의(P균<0.01).Ⅳ조적혈청NSE함량현저저우Ⅲ조,차이구유통계학의의.재관주30 min,경정맥혈양포화도승고,Ⅲ조여Ⅳ조차이무통계학의의(P>0.05).결론 국부뇌조직아저온연합니막지평정맥수주능현저감소토전뇌결혈재관주후혈청NSE표체,승고SjvO2,감경결혈재관주손상소치적뇌수종.
Objective To explore the protection effect and mechanism of sub-hypothermia combined with nimodipine injection on global cerebral ischemic/repeffusion (I/R) injury. Methods Twenty-four healthy New Zealand rabbits were randomly divided into normal control group (group Ⅰ) ,normal thermal I/R group (group Ⅱ), sub-hypothermia I/R group (group Ⅲ), sub-hypothermia combined with nimodipine injection I/R group(group Ⅳ). The model was established by bilateral common carotid arteries occlusion for 30 min combined with systemic hypotension. Except the normal control group,the rabbits underwent ischemia for 30 min and were reperfused for 3 hours. Local cerebral sub-hypothermal was given to group Ⅲ at the same time of ischemia and reperfusion for 3 hours. The local cerebral sub-hypothermal combined with 10 μg·kg-1·h-1 nimodipine intravenous injection was given to group Ⅳ. The temperature of the tympanic membrane, mean arterial pressure(MAP) and central venous pressure(CVP) were routinely recorded. Artery blood and oxygen saturation of jugular vein(SjvO2) were detected before ischemia, ischemia for 30 min, reperfusion for 30,60, 120,180 min. Cerebral water contant was calculated after sacrifice of rabbits. ELISA method was used to detect the content of serum neurons specific enolase(NSE). Results The water content was highest in group Ⅱ, and lowest in group Ⅳ. The content of NSE was increased significantly after reperfusion for 60 min[(14.07±0.67) μg/L] ,and reached the highest level after reperfusion for 120 min[(18.53±0.85)μg/L], but the SjvO2 was reduced[(66±7.6)%]. The content of serum NSE was reduced after reperfusion for 60 min[(7. 27±0.25) μg/L] and for 180 min by sub-hypothemia treatment [(9.17±0.57) μg/L], compared with group Ⅱ ,the difference was significant(all P<0.01). The decreased level of the serum NSE was more significant in group Ⅳ than that in group Ⅲ. However ,the difference of increased SjvO2 was not significant between these two groups after reperfusion for 30 min (P>0.05). Conclusion The local cerebral sub-hypothermia combined with nimodipine intravenous injection can significantly reduce the serum NSE content, increase the SjvO2, and attenuate the cerebral edema after I/R injury in rabbit.
