Renin-Angiotensin-System-dependent alterations of respiratory chemosensitivity in Acute Respiratory Distress Syndrome

急性呼吸窘迫综合征中肾素-血管紧张素系统依赖性呼吸化学敏感性改变

• 批准号: 454644812
• 负责人: Professor Dr. Swen Hülsmann
• 金额: --
• 依托单位: Klinik für Anästhesiologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/454644812?language=en
• 关键词: Renin; Angiotensin; System; dependent; alterations

The acute respiratory distress syndrome (ARDS) is a critical clinical condition of acute hypoxemic respiratory failure with non-cardiogenic pulmonary edema and diffuse lung inflammation leading to severely impaired exchange oxygen and carbon dioxide. Many ARDS patients show a high respiratory drive that appears to be disconnected from the actual blood gas status. The objective of the project is to test the hypothesis that ARDS accompanying alterations of Renin-Angiotensin-System (RAS) signaling are involved in the apparent dysregulation of chemosensitive control of breathing. Using electrophysiological techniques, the project aims to clarify how the responsiveness of chemosensitive cell populations are altered in mouse models of ARDS. The expected results should improve our understanding of the specific role of the renin-angiotensin system in peripheral and central respiratory chemosensitivity and advance our knowledge of pathophysiological alteration of breathing control in ARDS or SARS patients but also might lead to new therapeutically concepts for intensive care and treatment of patients with acute lung injury.

急性呼吸窘迫综合征（ARDS）是一种急性低氧性呼吸衰竭的危重临床病症，伴有非心源性肺水肿和弥漫性肺部炎症，导致氧气和二氧化碳交换严重受损。许多呼吸窘迫综合征患者表现出高度的呼吸动力，这似乎与实际的血气状态脱节。该项目的目的是检验以下假设，即ARDS伴随的肾素-血管紧张素系统（RAS）信号转导的改变涉及呼吸的化学敏感性控制的明显失调。利用电生理学技术，该项目旨在阐明在ARDS小鼠模型中化学敏感细胞群体的反应性是如何改变的。预期的结果应提高我们的理解的特定作用的肾素-血管紧张素系统在外周和中央呼吸系统的化疗敏感性和推进我们的知识呼吸控制的病理生理学改变在ARDS或SARS患者，但也可能导致新的治疗概念重症监护和治疗急性肺损伤患者。