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Worsening of lung perfusion to tissue density distributions during early acute lung injury
Journal article   Open access   Peer reviewed

Worsening of lung perfusion to tissue density distributions during early acute lung injury

Gabriel C Motta-Ribeiro, Tilo Winkler, Eduardo L V Costa, Nicolas de Prost, Mauro R Tucci and Marcos F Vidal Melo
Journal of applied physiology (1985), Vol.135(2), pp.239-250
08/01/2023
DOI: 10.1152/japplphysiol.00028.2023
PMCID: PMC10393328
PMID: 37289955
url
https://www.ncbi.nlm.nih.gov/pmc/articles/10393328View
Open Access

Abstract

Lung perfusion magnitude and distribution are essential for oxygenation and, potentially, lung inflammation and protection during acute respiratory distress syndrome (ARDS). Yet, perfusion patterns and their relationship to inflammation are unknown pre-ARDS. We aimed to assess perfusion/density ratios and spatial perfusion-density distributions and associate these to lung inflammation, during early lung injury in large animals at different physiological conditions caused by different systemic inflammation and positive end-expiratory pressure (PEEP) levels. Sheep were protectively ventilated (16-24 h) and imaged for lung density, pulmonary capillary perfusion ( Nitrogen-saline), and inflammation ( F-fluorodeoxyglucose) using positron emission and computed tomography. We studied four conditions: permissive atelectasis (PEEP = 0 cmH O); and ARDSNet low-stretch PEEP-setting strategy with supine moderate or mild endotoxemia, and prone mild endotoxemia. Perfusion/density heterogeneity increased pre-ARDS in all groups. Perfusion redistribution to density depended on ventilation strategy and endotoxemia level, producing more atelectasis in mild than moderate endotoxemia ( = 0.010) with the oxygenation-based PEEP-setting strategy. The spatial distribution of F-fluorodeoxyglucose uptake was related to local Q/D ( < 0.001 for Q/D group interaction). Moderate endotoxemia yielded markedly low/zero perfusion in normal-low density lung, with Nitrogen-saline perfusion indicating nondependent capillary obliteration. Prone animals' perfusion was remarkably homogeneously distributed with density. Lung perfusion redistributes heterogeneously to density during pre-ARDS protective ventilation in animals. This is associated with increased inflammation, nondependent capillary obliteration, and lung derecruitment susceptibility depending on endotoxemia level and ventilation strategy. Perfusion redistribution does not follow lung density redistribution in the first 16-24 h of systemic endotoxemia and protective tidal volume mechanical ventilation. The same oxygenation-based positive end-expiratory pressure (PEEP)-setting strategy can lead at different endotoxemia levels to different perfusion redistributions, PEEP values, and lung aerations, worsening lung biomechanical conditions. During early acute lung injury, regional perfusion-to-tissue density ratio is associated with increased neutrophilic inflammation, and susceptibility to nondependent capillary occlusion and lung derecruitment, potentially marking and/or driving lung injury.
 Acute Lung Injury Animals Endotoxemia Fluorodeoxyglucose F18 Inflammation Lung - blood supply Nitrogen Perfusion Pneumonia Pulmonary Atelectasis Respiratory Distress Syndrome Sheep

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