BREATHLESSNESS

呼吸困难

• 批准号: 7377362
• 负责人: NAUSHERWAN K BURKI
• 金额: $ 0.12万
• 依托单位: UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7377362
• 关键词: BREATHLESSNESS

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. Dyspnea, an unpleasant sensation of difficulty in breathing, is a common symptom in patients with with cardiopulmonary diseases, but the underlying mechanisms are unclear. Amongst the various neural pathways, unmyelinated vagal C fibers arising from the lungs and airways have been implicated. The long term objectives are to increase understanding of the mechanisms of dyspnea and specifically the role of pulmonary C fibers. Adenosine is a commonly used therapeutic intravenous drug for treatment of supraventricular tachycardia; it has been frequently reported to cause dyspnea. Recent studies from our laboratory reported the first evidence showing that adenosine stimulates pulmonary C fiber receptors in anesthetized rats. Preliminary human studies from our laboratory indicate that intravenous adenosine causes dyspnea and increases ventilation, and neither effect is associated with bronchoconstriction. Adenosine is known to increase ventilation by stimulating the carotid body chemoreceptors; such reflex stimulation would increase central motor command and could lead to the development of dyspnea. Our hypothesis is that adenosine causes dyspnea by direct activation of the pulmonary C fiber, and it is not an indirect effect related to the increase in ventilation. The specific aims of the proposed study are: 1. To determine the latency and magnitude of the dyspneic response, change in airway resistance, and ventilatory response to intravenous injection of adenosine in normal subjects and stable asthmatics, 2. To evaluate the effects of pretreatment with theophylline, an adenosine receptor antagonist, on the intensity of dyspnea and the ventilatory effects of intravenous adenosine; 3. To examine whether directly blocking pulmonary C fibers with inhaled lidocaine abolishes the sensation of dyspnea induced by adenosine in these subjects/patients; 4. To investigate if pretreatmeni with 100% 0;, by reducing carotid chemoreceptor sensitivity, alters the dyspnogenic and ventilatory effects of intravenous adenosine. These studies should bring a better understanding of the underlying mechanism of adenosine-induced dyspnea and the role of bronchopulmonary C fibers.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。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。列出的机构适用于该中心，这不一定是调查员的机构。呼吸困难是呼吸困难的一种不愉快的感觉，是心肺疾病患者的常见症状，但基本机制尚不清楚。在各种神经途径中，涉及由肺和气道引起的无髓的迷走神经纤维。长期目标是增加对呼吸困难机制，尤其是肺C纤维的作用的理解。腺苷是一种常用的治疗性静脉注射药，用于治疗上心动过速。经常据报道会引起呼吸困难。我们实验室的最新研究报告了第一个证据表明，腺苷刺激麻醉大鼠中的肺C纤维受体。我们实验室的初步人类研究表明，静脉注射腺苷会引起呼吸困难并增加通风，并且两者都与支气管收缩有关。已知腺苷通过刺激颈动体化学感受器来增加通风。这种反射刺激会增加中央运动的命令，并可能导致呼吸困难的发展。我们的假设是，腺苷通过直接激活肺C纤维引起呼吸困难，并且与通气增加无关。 拟议的研究的具体目的是：1。确定呼吸困难反应的潜伏期和幅度，气道阻力的变化以及对正常受试者静脉注射腺苷注入腺苷的通气反应和稳定的哮喘患者2。评估辅导层抗浓度及其含量及其含量及其含量及其含量的浓度及其含量的影响，并评估腺苷的疗程的影响。腺苷； 3。检查是否直接阻断用吸入的利多卡因阻止肺C纤维消除这些受试者/患者腺苷诱导的呼吸困难的感觉； 4。通过降低颈动脉化学感受器的敏感性来研究以100％0;的预处理，以改变静脉注射腺苷的营养性和通气作用。这些研究应更好地了解腺苷诱导的呼吸困难的潜在机制和支气管肺C纤维的作用。