HYPOXIA OF BRAIN TISSUE SLICES

脑组织切片缺氧

• 批准号: 3398707
• 负责人: GEORGE G SOMJEN
• 金额: $ 14.86万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1982
• 资助国家: 美国
• 起止时间: 1982-07-01 至 1988-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3398707
• 关键词: acid base balance; antidromic impulse; bioenergetics; cerebral ischemia /hypoxia; chronic brain damage; electrophysiology; free radicals; lactates; membrane permeability; neural inhibition; neural transmission; neuropharmacology; neurotransmitters; oxidizing agents; pathologic process; synapses

This project is designed to study the pathophysiology of acute cerebral hypoxia, as well as the aftereffects of exposure to hypoxia. The intent is to discover the effect of oxygen insufficiency itself, as distinct from effects mediated by changes of cerebral circulation. Slices of cerebral tissue will be maintained in vitro and exposed to hypoxia of varying degree and duration. The conditions will be defined in which reversible and irreversible changes of synaptic function occur. Tissue pH and other ion concentrations will be measured with ion selective microelectrodes. Tissue pO2 will be determined by polarography. Membrane properties of reversibly and irreversibly impaired neurons will be determined by intracellular methods and by voltage clamping. The roles of ions, of pH, and of post-hypoxic excess oxidant in influencing recovery will be studied. The possible protective effect of nutrients, metabolites and drugs against hypoxic damage will be determined. Findings in vitro will be compared with observations on intact brains in experiments performed in cooperation with Dr. Sylvia. Hypoxic changes of interstitial ions and of electrophysiological function will be related to biochemical changes. The chronic aftereffects of exposure to hypoxia will also be studied. Altered neuronal function caused by severe but transient oxygen deprivation will be determined as well as possible adaptation to prolonged, moderate lack of oxygen.

本项目旨在研究急性脑梗死的病理生理学， 缺氧，以及暴露于缺氧的后遗症。 目的是 发现氧气不足本身的影响，与 脑循环变化介导的效应。 将脑组织切片保存在体外并暴露于 不同程度和持续时间的缺氧。 这些条件将在 突触功能发生可逆和不可逆的变化。 组织pH值和其他离子浓度将采用离子选择性电极测量。 微电极 将通过极谱法测定组织pO2。 膜 可逆性和不可逆性受损神经元的特性将被 通过细胞内方法和电压箝位来确定。 的作用 离子、pH值和缺氧后过量氧化剂对恢复的影响 将被研究。 营养物质、代谢物、 并将确定抗缺氧损伤的药物。 体外结果 将与实验中对完整大脑的观察结果进行比较 与西尔维娅医生合作完成的 间质性低血压改变 离子和电生理功能将与生化 变化 暴露于缺氧的慢性后遗症也将是 研究了 由严重但短暂的氧气引起的神经功能改变 将确定剥夺以及可能的适应长期， 中度缺氧。