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Long term recurrent hypoxia in developing rat attenuates respiratory responses to subsequent acute hypoxia: proposed mechanisms
Author(s) -
Moss Immanuela Ravé,
Laferrière André
Publication year - 2006
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.20.5.a1211-b
Subject(s) - hypoxia (environmental) , respiratory system , tidal volume , hypoxemia , medicine , weaning , hypoxic ventilatory response , control of respiration , respiratory minute volume , ventilation (architecture) , anesthesia , respiration , respiratory rate , oxygen , heart rate , chemistry , anatomy , blood pressure , mechanical engineering , engineering , organic chemistry
Following recurrent hypoxemia in children, some physiological dysfunctions persist, attributable to long‐lasting central effects of prior hypoxia. To investigate such effects and their mechanisms, male rats were exposed to FiO2 = 0.12 continuously for 7 h daily from p17 (representing early childhood) through p33 (representing adolescence), defined as recurrent hypoxia. Subsequently, respiratory responses during and following 20 min FiO2 = 0.12 were measured on p35 and p47. Control groups for early weaning and sex differences were also tested for respiratory responsiveness to acute hypoxia. Minute ventilation, respiratory frequency, tidal volume and respiratory drive (tidal volume/inspiratory time) were measured in unsedated animals using whole body plethysmography. Following recurrent hypoxia, male rats displayed an attenuation of ventilation, frequency and respiratory drive during hypoxia, and of all functions after hypoxia on both p35 and p47. There were no differences between test days during hypoxia, and greater attenuation of tidal volume and respiratory drive on p47 following hypoxia. No effect of sex on p35, and occasional effects of early weaning occurred on p35 and p47. Mechanisms of this long‐lasting attenuation in respiratory responsiveness to acute hypoxia following recurrent hypoxia include neuromodulatory plasticity and neuronal apoptosis. Such long‐lasting respiratory attenuation, if present in humans, may diminish the protection of children with a history of recurrent hypoxemia against future hypoxic events. Supported by the Canadian Institutes of Health Research and the Montreal Children's Hospital Research Institute.