{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:49:51Z","timestamp":1787017791901,"version":"build-2736575974"},"reference-count":61,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2013,4,15]]},"abstract":"<jats:p>\n                    Hyperbaric oxygen (HBO\n                    <jats:sub>2<\/jats:sub>\n                    ) stimulates presumptive central CO\n                    <jats:sub>2<\/jats:sub>\n                    -chemoreceptor neurons, increases minute ventilation (V\u0307\n                    <jats:sub>min<\/jats:sub>\n                    ), decreases heart rate (HR) and, if breathed sufficiently long, produces central nervous system oxygen toxicity (CNS-OT; i.e., seizures). The risk of seizures when breathing HBO\n                    <jats:sub>2<\/jats:sub>\n                    is variable between individuals and its onset is difficult to predict. We have tested the hypothesis that a predictable pattern of cardiorespiration precedes an impending seizure when breathing HBO\n                    <jats:sub>2<\/jats:sub>\n                    . To test this hypothesis, 27 adult male Sprague-Dawley rats were implanted with radiotelemetry transmitters to assess diaphragmatic\/abdominal electromyogram, electrocardiogram, and electroencephalogram. Seven days after surgery, each rat was placed in a sealed, continuously ventilated animal chamber inside a hyperbaric chamber. Both chambers were pressurized in parallel using poikilocapnic 100% O\n                    <jats:sub>2<\/jats:sub>\n                    (animal chamber) and air (hyperbaric chamber) to 4, 5, or 6 atmospheres absolute (ATA). Breathing 1 ATA O\n                    <jats:sub>2<\/jats:sub>\n                    initially decreased V\u0307\n                    <jats:sub>min<\/jats:sub>\n                    and HR ( Phase 1 of the compound hyperoxic ventilatory response). With continued exposure to normobaric hyperoxia, however, V\u0307\n                    <jats:sub>min<\/jats:sub>\n                    began increasing toward the end of exposure in one-third of the animals tested. Breathing HBO\n                    <jats:sub>2<\/jats:sub>\n                    induced an early transient increase in V\u0307\n                    <jats:sub>min<\/jats:sub>\n                    ( Phase 2) and HR during the chamber pressurization, followed by a second significant increase of V\u0307\n                    <jats:sub>min<\/jats:sub>\n                    \u22648 min prior to seizure ( Phase 3). HR, which subsequently decreased during sustained hyperoxia, showed no additional changes prior to seizure. We conclude that hyperoxic hyperpnea ( Phase 3 of the compound hyperoxic ventilatory response) is a predictor of an impending seizure while breathing poikilocapnic HBO\n                    <jats:sub>2<\/jats:sub>\n                    at rest in unanesthetized rats.\n                  <\/jats:p>","DOI":"10.1152\/japplphysiol.01326.2012","type":"journal-article","created":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T23:48:32Z","timestamp":1361490512000},"page":"1009-1020","source":"Crossref","is-referenced-by-count":25,"title":["A potential early physiological marker for CNS oxygen toxicity: hyperoxic hyperpnea precedes seizure in unanesthetized rats breathing hyperbaric oxygen"],"prefix":"10.1152","volume":"114","author":[{"given":"Raffaele","family":"Pilla","sequence":"first","affiliation":[{"name":"Department of Molecular Pharmacology &amp; Physiology, Hyperbaric Biomedical Research Laboratory, University of South Florida, Morsani College of Medicine, Tampa, 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