{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T05:40:10Z","timestamp":1792129210408,"version":"4.4.0"},"reference-count":70,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2007,1,26]],"date-time":"2007-01-26T00:00:00Z","timestamp":1169769600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,2]]},"abstract":"<jats:p>Inputs from central (brainstem) and peripheral (carotid body) respiratory chemoreceptors are coordinated to protect blood gases against potentially deleterious fluctuations. However, the mathematics of the steady\u2010state interaction between chemoreceptors has been difficult to ascertain. Further, how this interaction affects time\u2010dependent phenomena (in which chemoresponses depend upon previous experience) is largely unknown. To determine how central <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub> modulates the response to peripheral chemostimulation in the rat, we utilized an <jats:italic>in situ<\/jats:italic> arterially perfused, vagotomized, decerebrate preparation, in which central and peripheral chemoreceptors were perfused separately (i.e. dual perfused preparation (DPP)). We carried out two sets of experiments: in Experiment 1, we alternated steady\u2010state brainstem <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub> between 25 and 50 Torr in each preparation, and applied specific carotid body hypoxia (60 Torr <jats:italic>P<\/jats:italic><jats:sub>O2<\/jats:sub> and 40 Torr <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub>) under both conditions; in Experiment 2, we applied four 5 min bouts (separated by 5 min) of specific carotid body hypoxia (60 Torr <jats:italic>P<\/jats:italic><jats:sub>O2<\/jats:sub> and 40 Torr <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub>) while holding the brainstem at either 30 Torr or 50 Torr <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub>. We demonstrate that the level of brainstem <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub> modulates (a) the magnitude of the phrenic responses to a single step of specific carotid body hypoxia and (b) the magnitude of time\u2010dependent phenomena. We report that the interaction between chemoreceptors is negative (i.e. hypo\u2010additive), whereby a lower brainstem <jats:italic>P<\/jats:italic><jats:sub>CO2<\/jats:sub> augments phrenic responses resulting from specific carotid body hypoxia. A negative interaction may underlie the pathophysiology of central sleep apnoea in populations that are chronically hypocapnic.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.119594","type":"journal-article","created":{"date-parts":[[2006,11,3]],"date-time":"2006-11-03T01:34:21Z","timestamp":1162517661000},"page":"843-857","source":"Crossref","is-referenced-by-count":65,"title":["Brainstem <i>P<\/i><sub>CO2<\/sub> modulates phrenic responses to specific carotid body hypoxia in an <i>in situ<\/i> dual perfused rat preparation"],"prefix":"10.1113","volume":"578","author":[{"given":"Trevor A.","family":"Day","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard J. 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