{'fraction_non_alphanumeric': 0.06677018633540373, 'fraction_numerical': 0.033385093167701864, 'mean_word_length': 4.6535087719298245, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Tissue conduction of acid‐induced lung injury

Acid aspiration causes spatially extensive pulmonary edema. To determine injury spreading mechanisms in tissue, we established isolated blood‐perfused rat lungs that we held at pulmonary artery, left atrial and end‐expiratory pressures of 10, 3 and 5 cmH2O, respectively. Through an intra‐tracheal catheter that we wedged in the left lower lobe, we infused a solution of HCl (0.05N, 1 ml) containing Evans Blue (EB). After one hour, we immersed the inflated lungs in liquid N2. Then from the frozen lung, we recovered tissue for the right lung as a whole, but for the left lung from EB‐stained, or ‐unstained regions lying within 1 cm of the catheter tip. In the control right lung, blood‐free extravascular lung water (EVLW) was 3.3±0.1 g/g dry (mean±SE, n=3). In the left lung, EVLW were higher at 6±0.8 and 3.9±0.1 g/g dry, respectively for both EB‐stained and ‐unstained regions (n=3, P<0.05). By contrast, following treatment with the gap junction inhibitor, glycerrhetinic acid (2–10 μM), at EB‐stained regions of the left lung EVLW was similar to control at 6.1±0.8 g/g dry (n=3). However for EB‐unstained regions, EVLW was markedly diminished at 3.5±0.1 (n=3, P<0.05). We conclude, for lung injury caused by airway acid instillation: