Affiliations: [a] Department of Anesthesia and Intensive Care, Carl Gustav Carus University Hospital, Technische Universität Dresden, Dresden, Germany | [b] Department of Radiopharmaceutical and Chemical Biology, Institute of Radiopharmaceutical Cancer Research, Helmholtz-Zentrum, Dresden-Rossendorf, Dresden, Germany | [c] Department of Chemistry and Food Chemistry, Technische Universität Dresden, Dresden, Germany
Correspondence:
[*]
Corresponding author: Torsten Richter, M.D., Department of Anesthesia and Intensive Care, University Hospital Technische Universität Dresden, Fetscherstrasse 74, 01307 Dresden, Germany. Tel.: +49 351 4582785; Fax: +49 351 4584336; [email protected].
Note: [1] The study was conducted at Helmholtz-Zentrum Dresden-Rossendorf, Dresden, Germany.
Abstract:
INTRODUCTION: Gastric aspiration events are recognized as a major cause of pneumonitis and the development of acute respiratory distress syndrome. The first peak in the inflammatory response has been observed one hour after acid-induced lung injury in rats. The spatial pulmonary blood flow (PBF) distribution after an acid aspiration event within this time frame has not been adequately studied. We determined therefore PBF pattern within the first hour after acid aspiration.
METHODS: Anesthetized, spontaneous breathing rats (n = 8) underwent unilateral endobronchial hydrochlorid acid instillation so that the PBF distributions between the injured and non-injured lungs could be compared. The signal intensity of the lung parenchyma after injury was measured by magnetic resonance tomography. PBF distribution was determined by measuring the concentration of [68Ga]-radiolabeled microspheres using positron emission tomography.
RESULTS: Following acid aspiration, magnetic resonance images revealed increased signal intensity in the injured regions accompanied by reduced oxygenation. PBF was increased in all injured lungs (171 [150; 196], median [25%; 75%]) compared to the blood flow in all uninjured lungs (141 [122; 159], P = 0.0078).
CONCLUSIONS: From the first minute until fifty minutes after acid-induced acute lung injury, the PBF was consistently increased in the injured lung. These blood flow elevation was accompanied by significant hypoxemia.
