Riha, I.; Salameh, A.; Hoschke, A.; Raffort, C.; Koedel, J.; Rassler, B. Hypoxia-Induced Pulmonary Injury—Adrenergic Blockade Attenuates Nitrosative Stress and Inflammation but Not Pulmonary Edema. Preprints2024, 2024011506. https://doi.org/10.20944/preprints202401.1506.v1
APA Style
Riha, I., Salameh, A., Hoschke, A., Raffort, C., Koedel, J., & Rassler, B. (2024). Hypoxia-Induced Pulmonary Injury—Adrenergic Blockade Attenuates Nitrosative Stress and Inflammation but Not Pulmonary Edema. Preprints. https://doi.org/10.20944/preprints202401.1506.v1
Chicago/Turabian Style
Riha, I., Julia Koedel and Beate Rassler. 2024 "Hypoxia-Induced Pulmonary Injury—Adrenergic Blockade Attenuates Nitrosative Stress and Inflammation but Not Pulmonary Edema" Preprints. https://doi.org/10.20944/preprints202401.1506.v1
Abstract
Hypoxia can induce pulmonary edema (PE) and inflammation. Furthermore, hypoxia depresses left ventricular (LV) inotropy despite sympathetic activation. Here, we investigated the role of nitrosative stress and cardiovascular dysfunction in hypoxic lung injury. Additionally, we studied effects of adrenergic blockade (AB) on hypoxia-induced pulmonary injury. Eighty-six female rats were exposed for 72 h to normoxia or normobaric hypoxia and received infusions with NaCl, prazosin, propranolol or prazosin-propranolol combination. We evaluated hemodynamic function and performed histological and immunohistochemical analyses of the lung. Hypoxia significantly depressed LV but not right ventricular (RV) inotropic and lusitropic functions. AB significantly decreased LV function both in normoxia and hypoxia. AB effects on RV were weaker. Hypoxic rats showed signs of moderate PE and inflammation. This was accompanied by elevated levels of tumor necrosis factor (TNF) and nitrotyrosine, a marker of nitrosative stress in the lungs. In hypoxia, all types of AB significantly reduced both TNF and nitrotyrosine to normoxic levels. However, AB did not attenuate PE. Results suggest that hypoxia-induced sympathetic activation contributes to inflammation and nitrosative stress in the lungs but not to PE. We suggest that AB in hypoxia aggravates hypoxia-induced inotropic LV dysfunction and backlog into pulmonary circulation, thus promoting PE.
Keywords
Normobaric hypoxia; adrenergic blockade; pulmonary edema; pulmonary inflammation; tumor necrosis factor; nitrotyrosine; left and right ventricular catheterization
Subject
Medicine and Pharmacology, Anatomy and Physiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
