中华物理医学与康复杂志
中華物理醫學與康複雜誌
중화물리의학여강복잡지
CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
2011年
7期
481-483
,共3页
王芳%罗洪英%段小毛%王俊杰%方会龙
王芳%囉洪英%段小毛%王俊傑%方會龍
왕방%라홍영%단소모%왕준걸%방회룡
脑缺血再灌注%缺血后适应%缺血预适应
腦缺血再灌註%缺血後適應%缺血預適應
뇌결혈재관주%결혈후괄응%결혈예괄응
Cerebral ischemia%Reperfusion%Ischemic postconditioning%Ischemic preconditioning
目的 探讨缺血后适应与缺血预适应对大鼠脑缺血再灌注损伤的影响。方法 用大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注损伤模型。30只SD大鼠分为脑缺血再灌注模型组(模型组)、缺血后适应组及缺血预适应组,每组10只。以脑梗死体积、神经功能缺陷评分、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量评价缺血预适应与缺血后适应抗脑缺血再灌注损伤的作用。结果 缺血后适应组大鼠实验性局灶性脑缺血的梗死体积减少,神经行为改善(P<0.05),但作用弱于缺血预适应组(P<0.01)。脑组织匀浆生化指标检测,缺血后适应和预适应可以增强SOD活性,降低MDA含量,与模型组比较,差异有统计学意义(P<0.01)。结论 缺血后适应可减轻局灶性脑缺血再灌注大鼠脑的病理性损伤,但作用弱于缺血预适应。
目的 探討缺血後適應與缺血預適應對大鼠腦缺血再灌註損傷的影響。方法 用大腦中動脈線栓法製作大鼠跼竈性腦缺血再灌註損傷模型。30隻SD大鼠分為腦缺血再灌註模型組(模型組)、缺血後適應組及缺血預適應組,每組10隻。以腦梗死體積、神經功能缺陷評分、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量評價缺血預適應與缺血後適應抗腦缺血再灌註損傷的作用。結果 缺血後適應組大鼠實驗性跼竈性腦缺血的梗死體積減少,神經行為改善(P<0.05),但作用弱于缺血預適應組(P<0.01)。腦組織勻漿生化指標檢測,缺血後適應和預適應可以增彊SOD活性,降低MDA含量,與模型組比較,差異有統計學意義(P<0.01)。結論 缺血後適應可減輕跼竈性腦缺血再灌註大鼠腦的病理性損傷,但作用弱于缺血預適應。
목적 탐토결혈후괄응여결혈예괄응대대서뇌결혈재관주손상적영향。방법 용대뇌중동맥선전법제작대서국조성뇌결혈재관주손상모형。30지SD대서분위뇌결혈재관주모형조(모형조)、결혈후괄응조급결혈예괄응조,매조10지。이뇌경사체적、신경공능결함평분、초양화물기화매(SOD)활성화병이철(MDA)함량평개결혈예괄응여결혈후괄응항뇌결혈재관주손상적작용。결과 결혈후괄응조대서실험성국조성뇌결혈적경사체적감소,신경행위개선(P<0.05),단작용약우결혈예괄응조(P<0.01)。뇌조직균장생화지표검측,결혈후괄응화예괄응가이증강SOD활성,강저MDA함량,여모형조비교,차이유통계학의의(P<0.01)。결론 결혈후괄응가감경국조성뇌결혈재관주대서뇌적병이성손상,단작용약우결혈예괄응。
Objective To study the effects of ischemic postconditioning and ischemic preconditioning on cerebral ischemia-reperfusion injury following middle cerebral artery occlusion in rats.Methods A reversible focal cerebral ischemia-reperfusion injury was modeled using middle cerebral artery occlusion. Thirty male Sprague-Dawley rats were randomized into three groups (n = 10 in each group) : a cerebral ischemia-reperfusion group, an ischemic postconditioning group and an ischemic preconditioning group. The impairment of neurological function was scored and the infarct volume, the activity of superoxide dismutase and malondiadehyde (MDA) content were measured after the operation.Results In the ischemic postconditioning and preconditioning groups the neurological function was better and the infarction volume was significantly smaller compared with the model group. In the preconditioning group both infarction volume and neurological function were significantly better than in the postconditioning group. In the brain tissues of the preconditioning and postconditioning groups MDA content was lower, while the activity of superoxide dismutase was significantly higher than in the model group.Conclusions lschemic postconditioning can attenuate pathological injury induced by focal cerebral ischemia and repedusion. The neuroprotective effect induced by ischemic preconditioning is stronger than that induced by ischemic postconditioning.