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的增加导致 疾病或环境的改变对呼吸有深远的影响。它 认为脑干化学感受器主要负责 由氢离子的变化所激发， 二氧化碳与水在组织和活动的其他强烈 游离离子本研究基于以下假设： 介导的离子跨细胞膜的转运是 确定对大脑中呼吸化学感受器的刺激 茎我们建议通过实验来评估这一假设， 麻醉的猫和兔子，测量对 急性呼吸性酸中毒载体介导的抑制剂 钠/钾偶联氯离子交换将通过 通过脑干的脑脊液腔灌注 枕大池精确定位区域和细胞类型， 离子交换抑制剂将通过定量的方法制备， 免疫荧光显微术。离子转运抑制对 细胞外液pH值将在该部位测定， 化学感受器和对细胞内元素浓度的影响 电子探针显微分析。这项工作的目标是一个 了解负责骨髓的化学过程， 化学感受器在酸碱平衡期间控制呼吸中的作用 由急性或慢性呼吸衰竭引起的紊乱。