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.

引起动脉血液中二氧化碳浓度的增加 通过疾病或环境改变，对呼吸产生了深远的影响。它 认为脑干化学感受器主要负责 由氢离子变化刺激，由反应决定 二氧化碳在组织中的水和其他强烈的活性 解离的离子。这项研究基于载体的假设 离子跨细胞膜的介导的运输是基本步骤 确定大脑中呼吸学化学感受器的刺激 干。我们建议通过实验评估这一假设 麻醉猫和兔子，测量 急性呼吸酸中毒。载体介导的抑制剂 钠/钾耦合氯化物交换将由 通过 水库麦格纳。区域和细胞类型的精确定位 离子交换的抑制剂将通过定量进行 免疫荧光显微镜。离子传输抑制对 细胞外流体pH将在 化学感受器以及对细胞内元素浓度的影响 通过电子探针微分析。这项工作的目的是 了解负责髓质的化学过程 化学感受器在控制酸碱期间呼吸中的作用 急性或慢性呼吸衰竭造成的干扰。