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Anoxia‐induced respiratory arrest and autoresuscitation in rat pups exposed to dietary tryptophan deficiency
Author(s) -
Corcoran Andrea E,
Kinney Hannah C,
Nattie Eugene E
Publication year - 2012
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.26.1_supplement.704.23
Subject(s) - asphyxia , hypercapnia , sudden infant death syndrome , hypoxia (environmental) , serotonergic , serotonin , reflex , respiratory system , endocrinology , medicine , tryptophan , cardiorespiratory fitness , physiology , anesthesia , biology , chemistry , pediatrics , receptor , amino acid , oxygen , biochemistry , organic chemistry
Many Sudden Infant Death Syndrome cases are associated with abnormalities in the medullary serotonergic system. We hypothesize that these abnormalities impair infants from adequately responding to stresses, such as hypoxia and hypercapnia (asphyxia), which may be a consequence of rebreathing exhaled gases when in the prone positition. Asphyxia initiates a series of events that lead to a reflex known as autoresuscitation. To examine the role of a moderate depletion of serotonin (5HT) on autoresuscitation, we studied pups born from Sprague‐Dawley dams fed a diet partially deficient in tryptophan (~45%). Using head‐out plethysmography, we identified the cardiorespiratory responses to repeated episodes of anoxia (97% N 2 :3% CO 2 ) and the ability to autoresuscitate from anoxia‐induced respiratory arrest. At each age studied (P5, P8, P12) tryptophan deficient pups had a similar level of autoresuscitation failure as control. We then examined the effect of “pretreatment” with prior post‐natal chronic intermittent hypoxia (CIH) on the ability to autoresuscitate. CIH increased the ability of control pups to autoresuscitate but had no effect on survival in tryptophan deficient pups (P=0.042; Chi‐square). This suggests that CIH improves the ability to autoresuscitate from anoxia‐induced respiratory arrest, likely through a 5HT dependent mechanism. (NIH National Institute of Child Health and Development HD36379)