{'fraction_non_alphanumeric': 0.03571428571428571, 'fraction_numerical': 0.0121580547112462, 'mean_word_length': 4.652360515021459, 'pattern_counts': {'":': 0, '<': 0, '<?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}}
TNF-alpha in smoke inhalation lung injury.

Adult respiratory distress syndrome is a major cause of morbidity in fire victims. Tumor necrosis factor-alpha(TNF-alpha) is edematogenic and has been associated with the etiology of other forms of adult respiratory distress syndrome. In the sheep lymph fistula model, we measured TNF-alpha after 48 (n = 7) or 128 (n = 3) breaths of cotton smoke and compared this with sham controls (n = 5) or controls in which left atrial pressure was elevated to 20 mmHg (n = 5) to increase lymph flow in the absence of inflammation. Smoke induced a rise in lymph flow and pulmonary arterial pressure with either no fall in lymph-to-plasma protein ratio (128 breaths) or a modest fall in lymph-to-plasma protein ratio (48 breaths), consistent with a change in microvascular permeability as well as a rise in microvascular pressure. Lymph concentration of TNF-alpha fell in both groups, although lymph flux (concentration x flow) transiently rose in both. In neither case did TNF-alpha flux exceed that induced by left atrial pressure elevation. TNF-alpha was detectable in only one out of five sheep in alveolar lavage. Thus, by utilizing a sensitive and specific radioimmunoassay, we were unable to demonstrate a role for TNF-alpha in smoke-induced microvascular lung injury in sheep.