中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
8期
984-986
,共3页
李国风%张建新%骆海坤%李兰芳%张勤增%解丽君%李立萍%郝娜%王薇薇
李國風%張建新%駱海坤%李蘭芳%張勤增%解麗君%李立萍%郝娜%王薇薇
리국풍%장건신%락해곤%리란방%장근증%해려군%리립평%학나%왕미미
胱硫醚-β合酶%脑缺血%氨基氧乙酸
胱硫醚-β閤酶%腦缺血%氨基氧乙痠
광류미-β합매%뇌결혈%안기양을산
Cystathionine beta-synthase%Cerebral ischemia%Aminooxoacetic acid
目的 评价氨基氧乙酸对大鼠局灶性脑缺血损伤的影响.方法 健康雄性SD大鼠80只,体重250~280 g,月龄2.5个月,采用随机数字表法,将其随机分为5组(n=16):假手术组(S组)、脑缺血组(Ⅰ组)、低、中、高剂量氨基氧乙酸组(AL组、AM组和AH组).Ⅰ组、AL组、AM组和AH组采用线栓法(阻塞大脑中动脉)制备大鼠局灶性脑缺血损伤模型.AL组、AM组和AH组于缺血3h时分别腹腔注射氨基氧乙酸25、50、100 μmol/kg,S组和Ⅰ组给予等容量生理盐水1ml/kg.每组于给予氨基氧乙酸后21 h时取8只大鼠,进行神经功能缺陷评分,然后处死大鼠,取脑组织,分离皮层、海马、纹状体,测定胱硫醚-β合酶( CBS)活性.每组于给予氨基氧乙酸后21 h时处死另外8只大鼠,取脑组织,测定脑梗死体积.结果 与S组比较,Ⅰ组神经功能缺陷评分、皮层和海马CBS活性升高,脑梗死体积扩大(P<0.05),纹状体CBS活性差异无统计学意义(P>0.05);与Ⅰ组比较,AM组和AH组神经功能缺陷评分、皮层和海马CBS活性降低,脑梗死体积缩小,纹状体CBS活性差异无统计学意义(P>0.05);AL组上述指标差异无统计学意义(P>0.05).结论 氨基氧乙酸可减轻大鼠局灶性脑缺血损伤,其机制与抑制CBS活性,减少H2S生成有关.
目的 評價氨基氧乙痠對大鼠跼竈性腦缺血損傷的影響.方法 健康雄性SD大鼠80隻,體重250~280 g,月齡2.5箇月,採用隨機數字錶法,將其隨機分為5組(n=16):假手術組(S組)、腦缺血組(Ⅰ組)、低、中、高劑量氨基氧乙痠組(AL組、AM組和AH組).Ⅰ組、AL組、AM組和AH組採用線栓法(阻塞大腦中動脈)製備大鼠跼竈性腦缺血損傷模型.AL組、AM組和AH組于缺血3h時分彆腹腔註射氨基氧乙痠25、50、100 μmol/kg,S組和Ⅰ組給予等容量生理鹽水1ml/kg.每組于給予氨基氧乙痠後21 h時取8隻大鼠,進行神經功能缺陷評分,然後處死大鼠,取腦組織,分離皮層、海馬、紋狀體,測定胱硫醚-β閤酶( CBS)活性.每組于給予氨基氧乙痠後21 h時處死另外8隻大鼠,取腦組織,測定腦梗死體積.結果 與S組比較,Ⅰ組神經功能缺陷評分、皮層和海馬CBS活性升高,腦梗死體積擴大(P<0.05),紋狀體CBS活性差異無統計學意義(P>0.05);與Ⅰ組比較,AM組和AH組神經功能缺陷評分、皮層和海馬CBS活性降低,腦梗死體積縮小,紋狀體CBS活性差異無統計學意義(P>0.05);AL組上述指標差異無統計學意義(P>0.05).結論 氨基氧乙痠可減輕大鼠跼竈性腦缺血損傷,其機製與抑製CBS活性,減少H2S生成有關.
목적 평개안기양을산대대서국조성뇌결혈손상적영향.방법 건강웅성SD대서80지,체중250~280 g,월령2.5개월,채용수궤수자표법,장기수궤분위5조(n=16):가수술조(S조)、뇌결혈조(Ⅰ조)、저、중、고제량안기양을산조(AL조、AM조화AH조).Ⅰ조、AL조、AM조화AH조채용선전법(조새대뇌중동맥)제비대서국조성뇌결혈손상모형.AL조、AM조화AH조우결혈3h시분별복강주사안기양을산25、50、100 μmol/kg,S조화Ⅰ조급여등용량생리염수1ml/kg.매조우급여안기양을산후21 h시취8지대서,진행신경공능결함평분,연후처사대서,취뇌조직,분리피층、해마、문상체,측정광류미-β합매( CBS)활성.매조우급여안기양을산후21 h시처사령외8지대서,취뇌조직,측정뇌경사체적.결과 여S조비교,Ⅰ조신경공능결함평분、피층화해마CBS활성승고,뇌경사체적확대(P<0.05),문상체CBS활성차이무통계학의의(P>0.05);여Ⅰ조비교,AM조화AH조신경공능결함평분、피층화해마CBS활성강저,뇌경사체적축소,문상체CBS활성차이무통계학의의(P>0.05);AL조상술지표차이무통계학의의(P>0.05).결론 안기양을산가감경대서국조성뇌결혈손상,기궤제여억제CBS활성,감소H2S생성유관.
Objective To evaluate the effect of aminooxyacetic acid on focal cerebral ischemia injury in rats.Methods Eighty healthy male SD rats aged 2.5 month weighing 250-280 g were randomly divided into five groups( n = 16 each):sham operation group(group S),cerebral ischemia group(group Ⅰ),aminooxoacetic acid low,medium and high dose groups(groups AL,AM and AH ).Focal cerebral ischemia was induced by occlusion of middle cerebral artery using a nylon thread with rounding tip which was inserted into right internal carotid artery in groups I,AL,AM and AH.Intraperitoneal amincoxoacetic acid 25,50 and 100 μmol/kg were administered at 3 h of ischemia in groups AL,AM and AH respectively,while equal volume of normal saline 1 ml/kg were injected in groups S and I.Neurological function was assessed and scored (0= no deficit,4= unable to move,unconscious) in 8 rats at 21 h after aminooxyacetic acid administration in each group.The animals were then sacrificed and the brains were removed for determination of the cystathionine beta-synthase (CBS) activities in cortex,hippocampus and striatum corpora.The other eight rats of each group were sacrificed at 21 h after amincoxoacetic acid administration for determination of the cerebral infarct volume.Results Compared with group S,the neurological deficit scores and the CBS activities in cortex and hippocampus were significantly increased,the infarct volumes were significantly enlarged in group Ⅰ ( P < 0.05).Compared with group Ⅰ,the neurological deficit scores and the CBS activities in cortex and hippocampus were significantly decreased,the cerebral infarct volumes were significantly reduced in groups AM and AH (P < 0.05).There was no significant difference in the above-mentioned variables between groups AL and Ⅰ.Conclusion Aminooxoacetic acid can reduce focal cerebral ischemia injury by decreasing CBS activity and reducing H2 S production in rats.