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目的 :探讨缺血再灌注离体海马脑片的光信号改变特征 ,以及 L型 Ca2 +通道在脑缺血急性期损害中的作用。方法 :以缺氧缺糖 (OGD)方法诱导离体海马脑片缺血模型 ,采用自行构建的脑片透光检测系统 ,结合图象处理软件 Photoshop中的灰度分析检测脑片活性 ,并观察尼莫地平的作用。结果 :体外缺血使海马 CA1区域对光通透性增加 ,(7.5 9± 1.4 2 ) min达峰值 ,再灌后 (6 .37± 1.89) min恢复至本底水平 (n=15 slices) ;L型 Ca2 + 通道阻断剂尼莫地平 (0 .5 μmol/ L,n=10 slices;5 μmol/ L,n=9slices)对缺血所致的海马脑片透光度增加具有抑制作用。而高剂量组 (5 0 μmol/ L,n=11slices)则引起脑片透光度的增加 ,给药后 (2 5 .83± 6 .32 ) min达峰值 ;尼莫地平使海马脑片透光度增加 ,并呈剂量依赖性。结论 :离体脑片光通透性检测是一种简易 ,无创性的脑片活性评价方法 ;L型Ca2 +通道对于维持正常脑片活性具有重要意义 ,同时参与脑缺血急性期损害 ,作用具有双重性
Objective: To investigate the changes of optical signal in isolated rat hippocampal slices after ischemia-reperfusion and the role of L-type Ca2 + channels in the damage of acute cerebral ischemia. Methods: The model of hippocampal slices ischemia was induced by OGD and the activity of the slices was detected by gray scale analysis of image processing software Photoshop. The role of nimodipine. Results: In vitro ischemia increased the light permeability of hippocampal CA1 region (7.5 9 ± 1.4 2) min and reached the background level (n = 15 slices) after reperfusion (6.37 ± 1.89) min. Nimodipine (0.5 μmol / L, n = 10 slices; 5 μmol / L, n = 9 slices), an inhibitor of L-type Ca 2+ channel blocker, inhibited the increase of light transmittance of hippocampal slices induced by ischemia. However, the high dose group (50 μmol / L, n = 11 slices) caused an increase in light transmittance of the brain slices, reaching a peak value of (2.583 ± 6.32) min after administration. Nimodipine Luminosity increased in a dose-dependent manner. CONCLUSION: The in vitro brain slice light permeability test is a simple and noninvasive method for evaluation of brain activity. L-type Ca2 + channels play an important role in maintaining normal brain slice activity, and are involved in the damage of acute cerebral ischemia Duality