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Chronic intermittent hypoxia enhances habituation of the arousal response to acute hypoxia in developing rodents
Author(s) -
Darnall Robert A,
McWilliams Samuel,
Schneider Robert,
Tobia Christine
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1038.1
Subject(s) - habituation , arousal , hypoxia (environmental) , intermittent hypoxia , medicine , apnea , endocrinology , psychology , anesthesia , obstructive sleep apnea , audiology , neuroscience , oxygen , chemistry , organic chemistry
Arousal from sleep is a critical apnea recovery mechanism. Rat pups progressively increase their time to arousal (latency) during repeated exposures to hypoxia (short term habituation‐STH). We hypothesized that postnatal exposure to chronic intermittent hypoxia (CIH) would increase the mean time (over several acute hypoxia exposures) to arousal (long term habituation‐LTH) and would accentuate STH, especially at P15, an age equivalent to the time of the highest incidence of Sudden Infant Death Syndrome (SIDS). Pups and dam were exposed to CIH for a total of 25 days. Each pup was removed at P5, P15, and P25, and exposed to four 3‐min trials of 5% oxygen alternating with 6‐min periods of normoxia. During the hypoxia trials, arousal latency progressively increased in both the Control and CIH groups (STH‐P=0.024). There was a mean increase in latency only in the CIH group (LTH) (P=0.027), most prominent at P15 (<0.001) and P25 (P=0.007). At P15, but not at P5 or P25, the STH was also accentuated in the CIH group (P=0.039). There were corresponding effects on arousal thresholds (inspired O2 concentration and oxyhemoglobin saturation at the time of arousal) and complex effects on heart rate. These results support the hypothesis that exposure to chronic intermittent hypoxia accentuates habituation of the arousal response in developing rat pups, especially in early infancy, and is an important mechanism in SIDS. P01 HD36379.