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• W4378649755 abstract "Oxygen exchange between lungs and systemic tissues is essential for life. However, breathing air with high O 2 levels can cause pulmonary O 2 toxicity (POT)—a serious health hazard for divers breathing O 2 -enriched gases at high pressure, and patients undergoing hyperbaric O 2 therapy or breathing through a mechanical ventilator. POT occurs because increased rates of O 2 uptake ( J O2 ) across the air-blood barrier lead to high intracellular O 2 concentration in alveolar type I cells (AT I Cs), AT II Cs, and in pulmonary capillary endothelial cells (PCECs). In principle, one could reduce POT by reducing J O2 . According to Fick’s law of diffusion, one approach for reducing J O2 would be to decrease O 2 membrane permeability ( P M, O2 ). In this work, we focus on the possibility of mitigating POT damage by manipulating P M, O2 across the cell membranes of AT I Cs (which cover about 90% of the alveolar surface) and PCECs.Research from the past 25 years has shown that membrane proteins (e.g., some aquaporins, AQPs) can conduct gases, thereby increasing P M . Notably, AQP5, which has the highest-known CO 2 permeability, is highly expressed in the apical membrane of AT I Cs, and AQP1, which can conduct both CO 2 and O 2 , is highly expressed in both PCECs membranes.We hypothesize that AQP5 mediates a large fraction of J O2 across the alveolar wall, and AQP1 does the same across PCECs membranes. If true, genetic deletion of AQP5 and/or AQP1 should reduce POT. We test this hypothesis with (1) a normobaric POT mouse model in which male mice (wild type, WT, vs knockout, KO) are continuously exposed to >99% O 2 (“↑O 2 ”) vs room Air (“Air”) for ~60-72 hr; (2) KO mice genetically deficient in AQP5, AQP1, or both (double knockouts, dKO); and (3) POT assays, namely H 2 O/dry-lung weight ratio (marker of lung edema) and, on bronchiolar-alveolar lavage fluid, lactate dehydrogenase (LDH; marker for AT I C leakage) and protein (mainly albumin from blood plasma; marker for blood-gas-barrier leakiness).Consistent with previous work (on WT and AQP5- & AQP1-KOs) by others, “H 2 O/dry weight” data show no differences between WT and KOs under “↑O 2 ” conditions. This negative result is consistent with the observed 10–15% weight loss (presumably all H 2 O), which would have reduced net Starling forces for ultrafiltration, making AQP KOs irrelevant. However, preliminary LDH and protein data are consistent with the idea that the KO of AQP5 and/or AQP1 reduces POT. For “↑O 2 ,” the AQP1-KO (vs. WT) shows a weak trend towards lower LDH; AQP5-KO and dKO show trends so strong that mean LDH does not differ from WT/“Air.” Moreover, for “↑O 2 ,” AQP5-KO and dKO have protein levels markedly lower than WT/“↑O 2 .” Finally, for “↑O 2 ,” we observe a progressive decrease in mouse mortality in the sequence WT > AQP1-KO >> AQP5-KO > dKO. If the observed trends continue for larger N’s, our data would argue that AQP5 and AQP1 are protective for POT and point, for the first time, towards a role of AQP5 in conducting O 2 . ONR: N00014-20-1-2737 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process." @default.
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• W4378649755 date "2023-05-01" @default.
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• W4378649755 title "AQP5 and AQP1 as targets for prophylactic countermeasures for pulmonary hyperbaric oxygen toxicity" @default.
• W4378649755 doi "https://doi.org/10.1152/physiol.2023.38.s1.5734930" @default.
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