摘要
目的 观察己酮可可碱 (PTX)对沙鼠全脑缺血 /再灌注模型的作用效果 ,并对其作用机制进行初步探讨。方法 夹闭双侧颈动脉 ,诱导沙鼠全脑缺血 ,30分钟后松夹 ,再灌注 90min。在缺血诱导时 ,静脉给予 2 5mg·kg-1,或者 5 0mg·kg-1的PTX ;另一组于再灌注开始时静脉输注 2 5mg·kg-1的PTX。假手术组和对照组输入相同容积的 0 9%NaCl。再灌注开始时以 0 2 %伊文思兰 1ml·10 0g-1对所有沙鼠腹腔注射。实验结束时断头取脑 ,- 70℃冰箱保存 ,进行脑水肿定量、脑组织超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量测定及脑组织伊文思兰含量测定。结果 与对照组相比 ,在缺血诱导时或再灌注开始时输注 2 5mg·kg-1PTX明显减轻沙鼠脑水肿的程度 (P <0 0 5或0 0 1) ,脑组织脂质过氧化产物MDA含量显著降低 (P <0 0 5或 0 0 1) ,脑组织中SOD的活性明显升高 (P <0 0 5或 0 0 1) ,脑组织伊文思兰含量显著降低 (P <0 0 5或 0 0 1)。 5 0mg·kg-1PTX输注对沙鼠脑缺血 /再灌注损伤无保护作用 ,其中 3只沙鼠死于低血压休克。结论 在血液动力学稳定的前提下 ,PTX对脑缺血 /再灌注损伤的保护作用可能与其提高脑血流量 ,抑制超氧阴离子产生 。
Objective To evaluate the efficacy of PTX on the global cerebral ischemia reperfusion injuryMethods The global cerebral ischemia of gerbils was induced by clamping bilateral carotid arteries for 30 min , then declamping with the reperfusion lasting 90 min At the beginning of ischemia , PTX 25mg·kg -1 or 50mg·kg -1 was administered intravenously by mini infusion pump In another group , PTX 25mg·kg -1 was infused at the beginning of reperfusion In sham operated and control groups the same volume of 0 9% NaCl were infused 0 2% Even's blue 1ml·100g -1 was injected intraperitoneally At the end of experiment , The gerbils were decapitated to be preserved at -70℃ for measurement of water contents of whole hemispheres , cerebral superoxide dimutase (SOD) activity, malonyldialdehyde (MDA) content and Even's blue content Results As compared with those in control group, at the beginning of ischemia or reperfusion ,the administration with PTX 25mg·kg -1 significantly reduced the cerebral water content (P<0 05 or 0 01) MDA content in cerebrum was also significantly decreased (P<0 05 or 0 01) SOD activity in brain was increased markedly (P<0 05 or 0 01) , cerebral Even's blue content decreased obviously (P<0 05 or 0 01) However , infusion of PTX 50mg·kg -1 showed no protective effect on cerebral ischemia reperfusion injury and three gerbils in this group 50mg·kg -1 was died of hypotensive shock Conclusions PTX can protect the brain from ischemia reperfusion injury under the precondition of stable hemodynamics through improving cerebral blood flow , attenuating the production of superoxide anion and protecting vascular endotheliocyte
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2000年第3期162-164,共3页
Chinese Journal of Anesthesiology
