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

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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.