{'fraction_non_alphanumeric': 0.030285381479324403, 'fraction_numerical': 0.006988934187536401, 'mean_word_length': 5.658914728682171, '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}}
Hypocapnia aggravates hypoxia‐induced inhibition of alveolar Na‐transport

Hypercapnia that is often associated with ARDS inhibits alveolar fluid reabsorption by PKC‐dependent mechanisms. Also Hypocapnia seems to reduce lung fluid clearance. In both cases inhibition was associated with internalization of Na/K‐ATPase. Hypocapnia is a consequence of hyperventilation in hypoxia. Hypoxia also inhibits alveolar fluid clearance by decreasing Na/K‐ATPase‐ and Na‐channel dependent transepithelial Na transport. It is not known, however, how altered CO2 affects hypoxia‐induced alveolar reabsorption. To answer this question we exposed primary rat alveolar epithelial cells to acute and 24h of hypoxia with 5% and 3% CO2, and measured trans‐monolayer ion transport as short circuit currents (ISC) in Ussing chambers. We show here that inhibition of alveolar reabsorption by hypoxia and hypocapnia was additive. This effect was small after 30 min but well pronounced after 24h of treatment. Ion transport at both CO2‐levels was not affected by acetazolamide, an inhibitor of carbonic anhydrase. In contrast to earlier reports we found no hypocapnia‐induced inhibition of Na/K‐ATPase, i.e. ISC after apical permeabilization with amphotericin A, although there was a decrease in whole‐cell α1‐Na/K‐ATPase protein measured by Western blot. However, we found a decrease in amiloride‐sensitive ISC indicating inhibition of epithelial Na‐channels (ENaC), which was associated with a decrease in apical αENaC protein in hypoxia, which was enhanced by hypocapnia. Our results indicate that hypocapnia aggravates hypoxia‐induced inhibition of alveolar reabsorption which may enhance the risk of formation alveolar edema in hypoxia.