{'fraction_non_alphanumeric': 0.0377906976744186, 'fraction_numerical': 0.03997093023255814, 'mean_word_length': 4.666666666666667, '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}}
Depression of serotonin uptake by cultured endothelial cells exposed to high O2 tension.

Serotonin (5-hydroxytryptamine, 5-HT), a vasoactive amine, is removed from the pulmonary circulation by active transcellular transport into endothelial cells, followed by intracellular metabolism. Pulmonary uptake of 5-HT is depressed by high partial pressures of O2 (Po2). To characterized the cellular basis and mechanism for hyperoxic depression of lung 5-HT uptake, we evaluated the effect of high Po2 on 5-HT uptake by calf aortic endothelial cells in primary confluent monolayer. Cells were exposed to either 95% O2, or 14% O2 (controls) in 5% Co2 at 1 ATA for 20 or 42 h. Following exposure 5-[14C]HT (1 X 10-7 M) was added to the culture medium, and 5-HT uptake in pmol/10(6) cells was measured. Exposure to 95% O2 for 20 h or 42 H resulted in significant depression of 5-HT uptake by cultured endothelial cells, and uptakes remained significantly depressed 48 h after exposure to 95% O2 had ended. Inhibition of intracellular metabolism of 5-HT by iproniazid did not affect 5-HT uptake by control or O2-exposed endothelial cells. These results indicate that 1) high Po2 levels depress 5-HT uptake in endothelial cells by direct inhibition of the transcellular transport of 5-HT and 2) hyperoxic depression of 5-HT uptake in cultured endothelial cells is not readily reversible.