CO2 PRODUCTION AND VENTILATION IN COPD

慢性阻塞性肺病 (COPD) 中的二氧化碳产生和通气

基本信息

批准号：
7607626
负责人：
NAUSHERWAN K BURKI
金额：
$ 0.08万
依托单位：
UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
起止时间：
2007-04-01 至 2008-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7607626
关键词：
Acids Acute Affect Alveolar Alveolus Anatomy Bicarbonates Blood Blood capillaries Blood flow Breathing Buffers Carbohydrates Carbon Dioxide Chronic Obstructive Airway Disease Computer Retrieval of Information on Scientific Projects Database Diet Dietary Factors Diffuse Environmental air flow Equilibrium Esterified Fatty Acids Excretory function Exercise Failure Fatty acid glycerol esters Fever Funding Gases Glycogen Glycolysis Grant Human body Institution Lung Measures Metabolism Muscle Natural regeneration Obesity Patients Physiological Processes Production Property Research Research Personnel Resources Rest Source Stress Time United States National Institutes of Health base fatty acid metabolism oxidation respiratory

Acids Acute Affect Alveolar Alveolus Anatomy Bicarbonates Blood Blood capillaries Blood flow Breathing Buffers Carbohydrates Carbon Dioxide Chronic Obstructive Airway Disease Computer Retrieval of Information on Scientific Projects Database Diet Dietary Factors Diffuse Environmental air flow Equilibrium Esterified Fatty Acids Excretory function Exercise Failure Fatty acid glycerol esters Fever Funding Gases Glycogen Glycolysis Grant Human body Institution Lung Measures Metabolism Muscle Natural regeneration Obesity Patients Physiological Processes Production Property Research Research Personnel Resources Rest Source Stress Time United States National Institutes of Health base fatty acid metabolism oxidation respiratory

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项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. 1. Resting minute ventilation (Ve) is increased in normocapnic patients with COPD. 2. The ratio of CO2 production (VCO2) to resting Ve, is decreased in COPD 3. Whilst the relationship VCO2/arterial PCO2 in COPD is similar to normals, the relationship Ve/arterial PCO2 is decreased. 4. VCO2 is similar in normocapnic and hypercapnic COPD, but Ve/VCO2 is decreased in hypercapnic vs normocapnic COPD. 5. In contrast to normal subjects, both normocapnic and hypercapnic COPD patients respond to an added respiratory resistive load with a decrease in Ve and increase in end-tidal PCO2. SPECIFIC AIMS 1. In patients with normocapnic COPD, and in healthy normal subjects, measure resting Ve, VCO2, end-tidal CO2 and anatomic deadspace (Vdan) and alveolar deadspace (Vdalv) and examine the relationship amongst these parameters and in relationship to arterial PCO2 (PaCO2). 2. In patients with hypercapnic COPD, measure resting Ve, VCO2, end-tidal CO2, PaCO2, Vdan and Vdalv and examine the relationship amongst these parameters, and compare the results to normocapnic COPD patients. 3. In normocapnic and hypercapnic COPD patients, and in healthy normal subjects, examine the effects of an added resistive load on Ve, VCO2, and end-tidal CO2 to approximate the effects of acute exacerbations of COPD on these parameters. Ventilatory failure is associated with an increased arterial PCO2 (PaCO2). Arterial PaCO2 is determined by the balance between CO2 production and excretion from the body (VCO2). CO2 production is known to be increased in obesity (1), during exercise (2), fever, and with high carbohydrate diets (3, 4). The critical importance of CO2 has been recognized for a very long time: Were it not for the peculiar properties of carbon dioxide - a very weak acid and a gas - our bodies would be unable to survive in their present state" (5). A great deal is known about the production of CO2 (VCO2) by the human body as a natural physiologic process: CO2 is produced in muscle as a product of metabolism, diffuses rapidly into blood where it is transported to the lungs and excreted. The production of CO2 is dependent on three factors: metabolism, blood carriage mechanisms (acid/base, buffering mechanisms), and pulmonary excretion. Dietary factors which alter CO2 production are due to the differences between carbohydrates and fat: in glycolysis, 1 mol of CO2 is produced in regenerating 6 mol of ATP, whereas in non-esterified fatty acid metabolism 1 mol of CO2 is produced for 8 mol of ATP. Thus CO2 production is dependent on the balance between fat and glycogen oxidation, and can be influenced by dietary changes (3, 4). CO2 is carried in the blood as dissolved CO2 and [HCO3-] and is affected by the acid -base state. The excretion of CO2 by the lungs is considered primarily a function of ventilation, and complete equilibration is assumed between the PCO2 of capillary blood and the alveoli (2). However, under stress, such as during exercise, a disequilibrium occurs, related to the breathing cycle and blood flow. In healthy normal subjects there is a direct, curvilinear relationship between alveolar ventilation (VA) and arterial PCO2.

该副本是利用众多研究子项目之一由NIH/NCRR资助的中心赠款提供的资源。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构是对于中心，这不一定是调查员的机构。 1。静止通风（VE）的COPD患者增加。 2。二氧化碳产量（VCO2）与静止VE的比率在COPD中降低 3。虽然COPD中的关系VCO2/动脉PCO2与正态相似，但关系VE/动脉PCO2降低。 4。VCO2在Normocapnic和HyperPapnic COPD中相似，但VE/VCO2减少超icapnic vs normocapnic copd。 5。与正常受试者相反，正常型和高型COPD患者均对增加的呼吸电阻载荷有反应，而VE的降低和潮汐PCO2的增加。具体目标 1。在患有正常的COPD的患者中，在健康的正常受试者中，测量静息VE，VCO2，End Tidal CO2和解剖去皮空间（VDAN）和肺泡Deadspace（VDALV），并检查这些参数之间的关系以及与动脉PCO2（PACO2）之间的关系。 2。在患有静止COPD的患者中，测量静息VE，VCO2，End Tidal CO2，PACO2，VDAN和VDALV，并检查这些参数之间的关系，并将结果与正常的COPD患者进行比较。 3。在正常的和高含量COPD患者中，以及在健康的正常受试者中，检查了添加的电阻载荷对VE，VCO2和末端潮汐CO2的影响，以近似COPD急性加重对这些参数的影响。通气衰竭与动脉PCO2增加有关（PACO2）。动脉PACO2取决于二氧化碳产生与体内排泄之间的平衡（VCO2）。已知在运动（1），发烧和高碳水化合物饮食的肥胖症（1）中，二氧化碳的产生会增加（3，4）。二氧化碳的关键重要性已经很长一段时间了：是否不是因为二氧化碳的特性 - 一种非常弱的酸和气体 - 我们的身体将无法在当前状态下生存”（5）。关于人体在自然物理学过程中生产的二氧化碳（VCO2）的生产很广泛：co2的生产是一种自然的生产：co2是一种自然的生产，而co2却是一种产生的，co2是一种自然的生产。运输到肺部并排出。二氧化碳的产生取决于三个因素：代谢，血管机制（酸/碱，缓冲机制）和肺排泄。改变二氧化碳产生的饮食因素是由于碳水化合物和脂肪之间的差异引起的：在糖酵解中，在再生6摩尔的ATP中产生了1摩尔的二氧化碳，而在非层化脂肪酸代谢中，产生了8摩尔ATP的二氧化碳1摩尔1摩尔。因此，二氧化碳的产生取决于脂肪和糖原氧化之间的平衡，并且可能受饮食变化的影响（3，4）。二氧化碳作为溶解的二氧化碳和[HCO3-]中的血液中携带，并受酸碱态的影响。肺对CO2的排泄主要是通风的函数，并且假定毛细血管血液和肺泡的PCO2之间完全平衡（2）。但是，在诸如运动过程中的压力下，发生不平衡，与呼吸周期和血流有关。在健康的正常受试者中，肺泡通气（VA）和动脉PCO2之间存在直接的曲线关系。