PULMONARY AIRWAY AND VASCULAR FUNCTION ASSESSED BY HRCT

这一临床研究人员发展奖的目标是进一步 培养和培训一名独立的学术调查员 麻醉学和生理学。 这项研究将强调一种新技术，它可以 成人肺血管和气道的三维重建 活着。它有两个主要目标，第一个是建立当地的 传导气道对不同刺激的反应性，第二 确定肺血管和肺组织之间相互作用的程度 进行航空运输。具体的研究目标将首先针对 呼吸道对各种干预措施的反应的测试 与用于评估肺部疾病的标准呼吸道功能测试相关。 我们将测试区域呼吸道反应的机制和程度 不同大小的呼吸道在体内对支气管收缩的异质性 和支气管扩张剂，据报道有不同程度的收缩 部分气道树或通过不同的药理作用 小路。我还将能够评估肺部的影响 呼吸道树上的血管构筑。初步数据显示，即使是 相对较大的传导气道在以下情况下可能部分受阻 肺血管压力升高。我们假设这是 血管系统和气道树之间的相互作用将影响 呼吸道对内源性和外源性刺激的反应。至 检验这一假设，我们将量化呼吸道和局部血管 膨胀性及其相互作用的计算机重建 体内的气道树和血管树。我们还将确定 肺水肿加重对原位气道大小的进行性影响 和局部血管的尺寸。呼吸道和血管形态计量学 数据将应用于现有的呼吸道分析模型和 维管束树。我还将测试区域呼吸道反应的程度 通过呼吸道树对已知的生理刺激的异质性 在临床情况下使肺部状况恶化，特别是， 高血容量、低血容量、高碳酸血症和低氧。结果来自于 所有这些调查都将对我们的 临床对肺功能的理解和解读 布景。

The goal of this Clinical Investigator Development Award is to further development and training of an independent academic investigator in anesthesiology and physiology. The research will emphasize a new technology that permits three-dimensional reconstruction of the pulmonary airways and vessels in vivo. It has two primary objectives, the first to establish the local responsiveness of conducting airways to various stimuli, the second to determine the extent of interaction between the pulmonary vasculature and conducting airways. Specific research aims will first be directed toward the testing of the response of airways to a variety of interventions relevant to standard airways function tests used to assess lung disease. We will test the mechanism and extent of regional airway response heterogeneity in different size airways in vivo to bronchoconstrictors and bronchodilators that have been reported to differentially constrict portions the airway tree or work through different pharmacologic pathways. I will also be able to evaluate the effect of the pulmonary vasculature on the airway tree. Preliminary data have shown that even relatively large conducting airways can be partially obstructed when the pulmonary vasculature pressure is increased. We hypothesize that this interaction between the vasculature and airway tree will affect the responses of the airways to endogenous and exogenous stimulation. To test this hypothesis we will quantify airway and regional vascular distensibility and their interaction using computerized reconstruction of the in vivo airway and vascular trees. We will also determine the progressive effects of increasing pulmonary edema on in situ airway size and regional vascular dimensions. The airway and vascular morphometric data will be applied to existing analytical models of the airway and vascular tree. I will also test the extent of regional airway response heterogeneity through the airway tree to physiologic stimuli known to worsen pulmonary status in clinical conditions, specifically, hypervolemia, hypovolemia, hypercapnia, and hypoxia. The results from all of these investigations will have a significant impact on our understanding and interpretation of pulmonary function in the clinical setting.