{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,2]],"date-time":"2026-08-02T22:29:11Z","timestamp":1785709751028,"version":"3.56.0"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[1999,5,1]]},"abstract":"<jats:p>Cyclosporin A (CsA), an inhibitor of protein phosphatase 2B (calcineurin), has been shown to play a role in exocytosis and neutrophil mobility. Hyperoxia (&gt;95% oxygen for 72 h) causes lung injury and reduces lung compliance. This model is indicative of deficiencies in surfactant and elicits a vigorous immune response leading to further damage. We examined the effects of CsA on surfactant-secreting lung alveolar type II cells. CsA enhances ATP-stimulated increases in whole cell capacitance in the presence of 2 mM extracellular Ca<jats:sup>2+<\/jats:sup>. This measurement corresponds with increases in exocytosis. Because of its effect on the immune system and exocytosis from type II cells, CsA was examined for its protective effects against hyperoxia-induced lung damage in mice. We found that CsA (50 mg \u22c5 kg<jats:sup>\u22121<\/jats:sup>\u22c5 day<jats:sup>\u22121<\/jats:sup>) attenuated hyperoxia-induced reductions in lung compliance when administered before or during 72 h of &gt;95% oxygen ( P &lt; 0.05). CsA (10 mg \u22c5 kg<jats:sup>\u22121<\/jats:sup>\u22c5 day<jats:sup>\u22121<\/jats:sup>) also had a protective effect against hyperoxia-induced changes in neutrophil infiltration, capillary congestion, edema, and hyaline membrane formation. Wet lung weight-to-dry lung weight ratios did not show any significant changes after hyperoxia or hyperoxia plus CsA ( P &lt; 0.05). CsA may be useful to treat patients undergoing prolonged high-oxygen therapy and possibly other lung injuries.<\/jats:p>","DOI":"10.1152\/ajplung.1999.276.5.l786","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T23:52:46Z","timestamp":1514073166000},"page":"L786-L795","source":"Crossref","is-referenced-by-count":10,"title":["Cyclosporin A protects lung function from hyperoxic damage"],"prefix":"10.1152","volume":"276","author":[{"given":"E.","family":"Matthew","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Pun","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Simonich","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Iwamoto","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Dedman","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1006\/jsre.1996.4980"},{"key":"B2","doi-asserted-by":"crossref","first-page":"513","DOI":"10.1001\/archpedi.1959.02070010515017","volume":"97","author":"Avery M.","year":"1959","journal-title":"Am. 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