REPERFUSION AND ISCHEMIC BRAIN NECROSIS

描述（研究者摘要）：将对假设进行检查 缺血后，再灌注的定量水平会影响 导致神经元坏死。 建立了计算机控制的大鼠模型 其中可以维持恒定的脑灌注水平 压力，局部脑组织PO 2百分比，或任何其他连续 监测血流指数。 控制这些指数是可能的 在缺血期间以及在再灌注期间。 其定量 将通过间歇性测量记录与血流的关系， 通过H3清除的本地CBF。 在初步实验中，我们有 证明这种程度的控制是可行的时期， 缺血和再灌注超过一小时。 不断的侮辱， 会产生明显的组织损伤， 在不同的实验中，包括10 %，25%，50%，100%和150%， 缺血前水平 在这些不同水平上控制再灌注将 用于将由于再灌注引起的水肿加重与 上述缺血的严重程度，使得能够评估独立的 缺血和再灌注对神经元坏死和水肿的贡献。 在灌注固定后，通过计数 甲苯胺蓝染色切片中的死亡神经元，用500微米的 电极，允许损伤与病灶高度特异性相关， 血流量和PO 2百分比变化。 在同一切片中， 透明间隙和神经纤维空泡化也将被评估为 组织水肿 在平行实验中，新鲜组织比重将 用溴苯/煤油柱浮选法测定， 允许评估小于1 mm立方的小体积， 与电极位置相关。 的独立贡献 再灌注水平的神经元损伤和水肿，因此将有可能 定量评估。

DESCRIPTION (Investigator's Abstract): The hypothesis will be examined that following ischemia, the quantitative level of reperfusion affects the resulting neuronal necrosis. A computer-controlled rat model was developed in which it is possible to maintain a constant level of cerebral perfusion pressure, local brain tissue PO2 percent, or any other continuously monitored index of blood flow. It is possible to control these indices during ischemia as well as during reperfusion. Their quantitative relationship to blood flow will be documented by intermittent measurment of local CBF by H3 clearance. In preliminary experiments, we have demonstrated that this degree of control is feasible for periods of ischemia and of reperfusion of more than an hour. A constant insult which produces significant tissue damage will be followed by a period of constant reperfusion at different levels in different experiments, including 10 percent, 25 percent, 50 percent, 100 percent and 150 percent of the preischemic level. Control of reperfusion at these different levels will serve to uncouple the aggravation of edema due to reperfusion from the severity of the foregoing ischemia, enabling evaluation of the independent contributions of ischemia and reperfusion to neuronal necrosis and edema. Neuronal injury will be assessed after perfusion-fixation by counting of dead neurons in toluidine blue stained sections taken with 500 microns of the electrode, permitting highly specific correlation of injury with focal blood flow and PO2 percent changes. In the same sections, pericellular clear spaces and neuropil vacuolation will also be assessed as one index of tissue edema. In parallel experiments, fresh tissue specific gravity will be measured by the bromo-benzene/kerosene column flotation methdod, to permit assessment of small volumes less than 1 mm cubed also highly correlated with electrode location. The independent contributions of reperfusion level of neuronal injury and to edema will thus be possible to assess quantitatively.