{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T14:51:54Z","timestamp":1787496714307,"version":"build-2736575974"},"reference-count":48,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2014,10,1]]},"abstract":"<jats:p>\n                    We evaluated several methods for characterizing hypoxic chemosensitivity in the conscious rat. Adult Sprague-Dawley rats ( n = 30) were exposed to normobaric hypoxia [inspired oxygen fraction (Fio\n                    <jats:sub>2<\/jats:sub>\n                    ) 0.15, 0.12, and 0.09]. We measured ventilation (V\u0307e; barometric plethysmography), arterial oxygen saturation (SpO\n                    <jats:sub>2<\/jats:sub>\n                    ; pulse oximeter), and oxygen consumption and carbon dioxide production (V\u0307o\n                    <jats:sub>2<\/jats:sub>\n                    and V\u0307co\n                    <jats:sub>2<\/jats:sub>\n                    ; analysis of expired air). Linear regression analysis was used to define stimulus-response relationships. Testing was performed on 2 days to assess day-to-day reproducibility. Exposure to graded, steady-state hypoxia caused progressive reductions in SpO\n                    <jats:sub>2<\/jats:sub>\n                    that were, for any given Fio\n                    <jats:sub>2<\/jats:sub>\n                    , quite variable (SpO\n                    <jats:sub>2<\/jats:sub>\n                    range, 20\u201330%) among individuals. Hypoxia produced progressive increases in V\u0307e caused by increases in both tidal volume (VT) and breathing frequency. Hypoxia also increased the VT:inspiratory time (T\n                    <jats:sub>i<\/jats:sub>\n                    ) ratio, an indicator of central respiratory \u201cdrive.\u201d Hypoxia caused consistent, progressive declines in V\u0307o\n                    <jats:sub>2<\/jats:sub>\n                    , V\u0307co\n                    <jats:sub>2<\/jats:sub>\n                    , and core temperature (&gt;20% at the lowest SpO\n                    <jats:sub>2<\/jats:sub>\n                    ). We propose that optimal quantification of carotid chemoreceptor hypoxic sensitivity in the unanesthetized rodent should employ SpO\n                    <jats:sub>2<\/jats:sub>\n                    [a surrogate for arterial Po\n                    <jats:sub>2<\/jats:sub>\n                    (Pa\n                    <jats:sub>\n                      O\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    )] as the stimulus variable and the ventilatory equivalent for V\u0307co\n                    <jats:sub>2<\/jats:sub>\n                    (V\u0307e\/V\u0307co\n                    <jats:sub>2<\/jats:sub>\n                    ) and\/or mean inspiratory flow rate (VT\/T\n                    <jats:sub>i<\/jats:sub>\n                    ) normalized for V\u0307co\n                    <jats:sub>2<\/jats:sub>\n                    as the response variables. Both metrics take into account not only the important influence of a falling metabolic rate, but also SpO\n                    <jats:sub>2<\/jats:sub>\n                    , which represents the hypoxic stimulus at the carotid body. Because of the somewhat curvilinear nature of these responses, exposure to multiple levels of graded hypoxia provides the most complete characterization of hypoxic chemosensitivity.\n                  <\/jats:p>","DOI":"10.1152\/japplphysiol.00484.2014","type":"journal-article","created":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:43:00Z","timestamp":1406853780000},"page":"816-824","source":"Crossref","is-referenced-by-count":49,"title":["Quantifying hypoxia-induced chemoreceptor sensitivity in the awake rodent"],"prefix":"10.1152","volume":"117","author":[{"given":"Barbara J.","family":"Morgan","sequence":"first","affiliation":[{"name":"Department of Orthopedics and Rehabilitation and the John Rankin Laboratory of Pulmonary Medicine, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell","family":"Adrian","sequence":"additional","affiliation":[{"name":"Department of Orthopedics and Rehabilitation and the John Rankin Laboratory of Pulmonary Medicine, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa L.","family":"Bates","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and the John Rankin Laboratory of Pulmonary Medicine, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John M.","family":"Dopp","sequence":"additional","affiliation":[{"name":"Pharmacy Practice Division, School of Pharmacy, University of Wisconsin, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerome A.","family":"Dempsey","sequence":"additional","affiliation":[{"name":"Department of Population Health Sciences and the John Rankin Laboratory of Pulmonary Medicine, School of Medicine and Public Health, University of 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