IONIC BASIS OF ISCHEMIC CEREBRAL EDEMA

缺血性脑水肿的离子基础

• 批准号: 3413454
• 负责人: WISE YOUNG
• 金额: $ 13.98万
• 依托单位: NEW YORK UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1990
• 资助国家: 美国
• 起止时间: 1990-01-01 至 1992-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3413454
• 关键词: albumins; artery stenosis; atomic absorption spectrometry; blood brain barrier; blood pressure; brain edema; cerebral ischemia /hypoxia; electrolyte balance; electrophysiology; evoked potentials; furosemide; histology; immunocytochemistry; immunoglobulins; laboratory rat; mannitol; methylprednisolone; microelectrodes; neuroanatomy; neuropharmacology; neurophysiology

Large tissue net ionic shifts are associated with cerebral edema after middle cerebral artery occlusion (MCAo). The net ionic shifts correlate highly with water concentration changes with regression slopes of 150-160 mu moles/ml, close to plasma ionic concentrations, suggesting that ionic shifts caused edema since participation of other osmotic agents would reduce the slope. The causes of the net ionic shift are not known. We will test the hypotheses that (a) net ionic shifts result from differences in extracellular Na and K gradients driving Na entry and K loss and (b) glial K uptake causes different in the Na and K gradients. Extracellular Na and K will be measured with ion-selective microelectrodes after MCAo and compared with tissue ionic and water shifts. Albumen and IgG passage across the blood brain barrier, regional blood flow, blood pressure, and plasma ionic levels will be monitored. Ionic shifts will be investigated in rat cortical freeze lesions. Freezing disrupts glial cells, prevent K uptake, and thereby should reduce net ionic shift and edema. The effects of systemic furosemide, mannitol, and/or methylprednisolone on extracellular and tissue ionic shifts will be studied in the rat MCAo and cortical freeze models. Neurophysiological and morphological changes will be correlated with ionic shifts. These studies will clarify ionic mechanisms in edema, relate tissue ionic shifts to tissue damage, and establish rational bases for treating ionic edema in stroke.

大型组织净离子移位与脑水肿有关 脑动脉闭塞（MCAO）。 净离子移位相关 高度随水浓度变化，回归斜率为150-160 MU摩尔/ML，接近血浆离子浓度，表明离子 由于其他渗透剂的参与将会引起水肿 减少坡度。 净离子移位的原因尚不清楚。 我们 将检验（a）因差异而引起的（a）净离子变化的假设 在细胞外Na和K梯度中，驱动Na进入和K损失和（B） 神经胶质K摄取在Na和K梯度中引起不同。 细胞外 Na和K将用MCAO后的离子选择性微电极测量 并与组织离子和水移相比。 蛋白和IgG通道 跨过血脑屏障，区域血流，血压和 血浆离子水平将受到监测。 离子转移将被调查 在大鼠皮质冷冻病变中。 冻结破坏神经胶质细胞，防止K 吸收，从而减少净离子转移和水肿。 效果 全身速尿，甘露醇和/或甲基丙糖酮的 将在大鼠MCAO中研究细胞外和组织离子移位 皮质冻结模型。 神经生理和形态学变化将 与离子移位相关。 这些研究将阐明离子 水肿中的机制，将组织离子转移与组织损伤相关，然后 建立用于治疗中风离子水肿的理性基础。