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Three different groups of rat pups were exposed to 5 days of SH, starting at either postnatal age 1 (SH<jats:sub>1\u20135<\/jats:sub>), 11 (SH<jats:sub>11\u201315<\/jats:sub>), or 21 (SH<jats:sub>21\u201325<\/jats:sub>) days. Whole body plethysmography was used to assess the HVR and HCVR the day after SH exposure ended. The primary results indicated that 1) the HVR and HCVR of SH<jats:sub>11\u201315<\/jats:sub>rats were absent or attenuated (respectively) compared with age-matched rats raised in normoxia; 2) there was a profoundly high (\u223c84% of pups) incidence of unexplained mortality in the SH<jats:sub>11\u201315<\/jats:sub>rats; and 3) these phenomena were unique to the SH<jats:sub>11\u201315<\/jats:sub>group with no comparable effect of the SH exposure on the HVR, HCVR, or mortality in the younger (SH<jats:sub>1\u20135<\/jats:sub>) or older (SH<jats:sub>21\u201325<\/jats:sub>) rats. These results share several commonalities with the risk factors thought to underlie the etiology of sudden infant death syndrome, including 1) a vulnerable neonate; 2) a critical period of development; and 3) an environmental stressor.<\/jats:p>","DOI":"10.1152\/japplphysiol.00976.2013","type":"journal-article","created":{"date-parts":[[2013,12,27]],"date-time":"2013-12-27T02:40:46Z","timestamp":1388112046000},"page":"514-521","source":"Crossref","is-referenced-by-count":26,"title":["Vulnerability of neonatal respiratory neural control to sustained hypoxia during a uniquely sensitive window of development"],"prefix":"10.1152","volume":"116","author":[{"given":"C. A.","family":"Mayer","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Rainbow Babies &amp; Children's Hospital, Case Western Reserve University, Cleveland, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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