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

急性呼吸窘迫综合征（acute respiratory distress syndrome， ARDS）是急性低氧性呼吸衰竭合并非心源性肺水肿和弥漫性肺炎症导致氧气和二氧化碳交换严重受损的一种关键临床症状。许多ARDS患者表现出与实际血气状态脱节的高呼吸驱动。该项目的目的是验证ARDS伴随肾素-血管紧张素系统（RAS）信号的改变与呼吸化学敏感控制的明显失调有关的假设。利用电生理技术，该项目旨在阐明在ARDS小鼠模型中，化学敏感细胞群的反应性是如何改变的。预期的结果将提高我们对肾素-血管紧张素系统在周围和中枢呼吸化学敏感性中的具体作用的理解，并提高我们对ARDS或SARS患者呼吸控制的病理生理改变的认识，同时也可能为急性肺损伤患者的重症监护和治疗带来新的治疗理念。

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.