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Cerebral reperfusion injury 脑缺血-再灌注损伤
Objective:Study the effect of acusector on serum CK and LDH of cerebral ischemia reperfusion injury model in rats. 目的:研究电针对实验性脑缺血再灌注损伤大鼠血清中肌酸激酶(CK)和乳酸脱氢酶(LDH)的影响。
The destruction of BBB is an important mechanism of cerebral ischemia - reperfusion injury. 血脑屏障破坏是脑缺血再灌注(ischemia reperfusion，IR)脑损伤的重要的病理生理基础。
The results suggested that CGS has a protective effect on cerebral ischemia reperfusion injury in rats. 表明CGS对大鼠脑缺血再灌注损伤具有保护作用。
Objective To study the protective effect of Xuesaitong (XST) against cerebral ischemia reperfusion injury in rats. 摘要目的观察血塞通预处理对大鼠脑缺血再灌注损伤的保护作用。
Conclusions: We conclude that postischemia mild hyperglycemia do not aggravate cerebral ischemia reperfusion injury. 结论：缺血后轻度高血糖对缺血再灌注损伤无明显影响。
OBJECTIVE To study the protective effect of saponins from Anemarrhena asphodeloides Bge(SAaB)on cerebral ischemia- reperfusion injury in rats. 目的观察知母总皂苷(SAaB)对于大鼠脑缺血及再灌注损伤的保护作用。
Objective To study the expression of HSP70 and the effects of tetramethylpyrazine (TMP) on cerebral ischemic reperfusion injury (CIRI) in rats. 目的研究大鼠脑缺血?再灌注（CIRI）时热休克蛋白（HSP）70表达及川芎嗪对HSP70表达的影响。
Objective To study the protective effects of the total paeony glycoside (TPG) against global cerebral ischemia- reperfusion injury in gerbils. 目的观察赤芍总苷(TPG)对全脑缺血再灌注的保护作用。
Conclusion Flunarizine can promote the expression of HSP70 and may therefore protect the ischemic cerebral tissue after MCAO and reperfusion injury. 结论氟桂利嗪能促进HSP70表达，对缺血再灌注引起的受损脑组织起保护作用。
Methods: The method of ligating both common carotid arteries and vagus nerves was used to make acute cerebral ischemia reperfusion injury in mice. 方法:采用小鼠双侧颈总动脉和迷走神经结扎法制作脑缺血模型并观察NMS对其的影响。
METHOD The method of ligating both common carotids and vagus was used to make acute cerebral ischemia reperfusion injury in mice. 方法采用小鼠双侧颈总动脉和迷走神经结扎法制作脑缺血模型并观察脑舒宁对其的影响。
Extensive research has demonstrated that inflammatory reaction is the major pathophysiological mechanism of cerebral ischemia reperfusion injury. 大量研究证明炎症反应是脑缺血再灌注损伤的重要病理生理机制。
Role of LAMI - 116 in Reperfusion Injury of Rat EDL. L一粘附素单抗在缺血再灌注损伤中的作用
Walter C, Stephen R, Eric S, et al. Reperfusion injury after focal cerebral ischemia: the role of inflammation and therapeutic horizon[J]. Neurosurg, 1998,43(6): 1383. 韦登明;黄光照;张益鹄;等.;雷公藤内酯醇对大鼠局灶性脑缺血再灌注损伤保护作用的实验研究[J]
CONCLUSION:The iNOS derived-NO through cGMP activating ERK kinase/ERK/P90RSK cell signal pathway induces injury of nerve cells after cerebral ischemical reperfusion injury. 结论:脑缺血再灌注损伤时,诱导型一氧化氮合酶源性的一氧化氮可能通过环磷酸鸟苷激活了细胞外信号调节激酶激酶/细胞外信号调节激酶/P90RSK信号转导通路诱导了神经细胞的损伤。
CONCLUSION DK can protect myocardium against ischemia reperfusion injury. 结论dk对大鼠心肌缺血再灌注损伤有保护作用。
CINC not only involved in the reperfusion injury, but also acute rejection. CINC不仅参与再灌注损伤，而且参与急性排斥反应。
Myocardial reperfusion injury is a complex pathophysiological process. 心肌再灌注损伤是一个复杂的病理生理过程。
Animal experiment and clinical research show ,reactive oxygen species plays an important role in cerebral ischemia reperfusion,p47~(phox) is associated with ischemia reperfusion injury from p47~(phox) function in ROS generation. 动物实验和临床研究表明，活性氧在脑缺血再灌注中发挥了重要作用，从NAD(P)H氧化酶p47~(phox)在ROS的产生过程中的发挥重要作用可知，p47~(phox)与脑缺血再灌注损伤密切相关。