{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T03:08:59Z","timestamp":1787972939088,"version":"build-2784847793"},"reference-count":65,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["BX001681"],"award-info":[{"award-number":["BX001681"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017540","name":"HHS | NIH | NHLBI | NHLBI Division of Intramural Research","doi-asserted-by":"publisher","award":["2R15HL129209-02"],"award-info":[{"award-number":["2R15HL129209-02"]}],"id":[{"id":"10.13039\/100017540","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017540","name":"HHS | NIH | NHLBI | NHLBI Division of Intramural Research","doi-asserted-by":"publisher","award":["5R01HL152712"],"award-info":[{"award-number":["5R01HL152712"]}],"id":[{"id":"10.13039\/100017540","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2022,10,1]]},"abstract":"<jats:p> <jats:sup>99m<\/jats:sup>Tc-hexamethylpropyleneamine oxime (HMPAO) and <jats:sup>99m<\/jats:sup>Tc-duramycin in vivo imaging detects pulmonary oxidative stress and cell death, respectively, in rats exposed to &gt;95% O<jats:sub>2<\/jats:sub> (hyperoxia) as a model of acute respiratory distress syndrome (ARDS). Preexposure to hyperoxia for 48 h followed by 24 h in room air (H-T) is protective against hyperoxia-induced lung injury. This study\u2019s objective was to determine the ability of <jats:sup>99m<\/jats:sup>Tc-HMPAO and <jats:sup>99m<\/jats:sup>Tc-duramycin to track this protection and to elucidate underlying mechanisms. Rats were exposed to normoxia, hyperoxia for 60 h, H-T, or H-T followed by 60 h of hyperoxia (H-T + 60). Imaging was performed 20 min after intravenous injection of either <jats:sup>99m<\/jats:sup>Tc-HMPAO or <jats:sup>99m<\/jats:sup>Tc-duramycin. <jats:sup>99m<\/jats:sup>Tc-HMPAO and <jats:sup>99m<\/jats:sup>Tc-duramycin lung uptake was 200% and 167% greater ( P &lt; 0.01) in hyperoxia compared with normoxia rats, respectively. On the other hand, uptake of <jats:sup>99m<\/jats:sup>Tc-HMPAO in H-T + 60 was 24% greater ( P &lt; 0.01) than in H-T rats, but <jats:sup>99m<\/jats:sup>Tc-duramycin uptake was not significantly different ( P = 0.09). Lung wet-to-dry weight ratio, pleural effusion, endothelial filtration coefficient, and histological indices all showed evidence of protection and paralleled imaging results. Additional results indicate higher mitochondrial complex IV activity in H-T versus normoxia rats, suggesting that mitochondria of H-T lungs may be more tolerant of oxidative stress. A pattern of increasing lung uptake of <jats:sup>99m<\/jats:sup>Tc-HMPAO and <jats:sup>99m<\/jats:sup>Tc-duramycin correlates with advancing oxidative stress and cell death and worsening injury, whereas stable or decreasing <jats:sup>99m<\/jats:sup>Tc-HMPAO and stable <jats:sup>99m<\/jats:sup>Tc-duramycin reflects hyperoxia tolerance, suggesting the potential utility of molecular imaging for identifying at-risk hosts that are more or less susceptible to progressing to ARDS. <\/jats:p>","DOI":"10.1152\/ajplung.00126.2022","type":"journal-article","created":{"date-parts":[[2022,8,9]],"date-time":"2022-08-09T15:19:12Z","timestamp":1660058352000},"page":"L410-L422","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["In vivo molecular imaging stratifies rats with different susceptibilities to hyperoxic acute lung injury"],"prefix":"10.1152","volume":"323","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4887-604X","authenticated-orcid":false,"given":"Said H.","family":"Audi","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, Marquette University-Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Clement J. 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