CARBON DIOXIDE TRANSPORT AND CHEMOSENSITIVITY

二氧化碳传输和化学敏感性

• 批准号: 3340500
• 负责人: JEROME M ADAMS
• 金额: $ 14.82万
• 依托单位: UNIVERSITY OF VIRGINIA
• 依托单位国家: 美国
• 财政年份: 1983
• 资助国家: 美国
• 起止时间: 1983-04-01 至 1992-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3340500
• 关键词: brain metabolism; brain stem; bumetanide; carbon dioxide transport; cats; chemoreceptors; drug administration routes; electron probe spectrometry; fluorescence microscopy; ionophores; laboratory rabbit; pulmonary respiration; respiratory acidosis; sodium potassium exchanging ATPase

An increase in the carbon dioxide concentration in arterial blood caused by disease or altered environment has a profound effect on breathing. It is thought that the brain stem chemoreceptors primarily responsible are stimulated by hydrogen ion changes which are determined by the reaction of CO2 with water in the tissue and by the activities of other strongly dissociated ions. This study is based on the hypothesis that carrier mediated transport of ions across cell membranes is a cardinal step in determining the stimulus to the respiratory chemoreceptors in the brain stem. We propose to evaluate this hypothesis by experiments in anesthetized cats and rabbits, measuring the ventilatory response to acute respiratory acidosis. Inhibitors of carrier mediated sodium/potassium coupled chloride exchange will be administered by perfusing the cerebrospinal fluid space of the brain stem via the cisterna magna. Precise localization of region and cell type for the inhibitors of ion exchange will be made by quantitative immunofluorescence microscopy. The effect of ion transport inhibition on extracellular fluid pH will be determined at the site of the chemoreceptors and the effect on intracellular elemental concentrations by electron probe microanalysis. The objective of this work is an understanding of the chemical processes responsible for the medullary chemoreceptors role in controlling breathing during acid-base disturbances which result from acute or chronic respiratory failure.

动脉血中二氧化碳浓度升高引起 疾病或环境改变对呼吸有深远的影响。它 据认为，脑干化学感受器主要负责的是 由反应决定的氢离子变化刺激 CO2 与组织中的水以及其他强烈的活动 离解离子。本研究基于以下假设：载体 介导的离子跨细胞膜运输是一个重要步骤 确定对大脑中呼吸化学感受器的刺激 干。我们建议通过实验来评估这一假设 麻醉猫和兔子，测量通气反应 急性呼吸性酸中毒。载体介导的抑制剂 钠/钾耦合氯化物交换将由 通过灌注脑干的脑脊液空间 大水池。精确定位区域和细胞类型 离子交换抑制剂将通过定量制备 免疫荧光显微镜。离子转运抑制的影响 细胞外液 pH 值将在 化学感受器及其对细胞内元素浓度的影响 通过电子探针微量分析。这项工作的目标是 了解负责髓质的化学过程 化学感受器在酸碱过程中控制呼吸的作用 由急性或慢性呼吸衰竭引起的疾病。