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Hypoxia During Postnatal Development

Chronic hypoxia (CH) from birth blunts the ventilatory response to hypoxia in rats (21) and other species by unknown mechanisms. Although CH alters the VE response to hypoxia at the central nervous system level (99), CH from birth also affects maturation of carotid body type I cell O2 sensitivity. Type I cells dissociated from 11-day-old rats reared from birth in Fi02 0.12 demonstrated marked blimting of [Ca ]i responses to acute hypoxia compared with controls reared in noimoxia [Pg.264]

Marcel Dekker, Inc. 270 Madison Avenue. New York, NewYoric 10016 [Pg.264]

Fetal Arterial Oxygen Tension Implications for Carotid Chemoreceptor Maturation [Pg.265]

Fetal sheep carotid sinus nerve (13) and fetal rat type I cell [Ca ]i (68) responses to hypoxia are weak compared to mature postnatal responses. The consensus view is that carotid chemoreceptor O2 sensitivity is suppressed or adapted to the normally low Pa02 of the mammalian fetal environment ( 23-27 mmHg). Nature s design makes sense, from a teleological perspective to disable carotid chemoreceptor [Pg.265]


Schwieler GH. Respiratory regulation during postnatal development in cats and rabbits and some of its morphological substrates. Acta Physiol Scand Suppl 1968 304. Rigatto H. Control of ventilation in the newborn. Annu Rev Physiol 1984 46 661-667. Ackland GL, Noble R, Hanson MA. Red nucleus inhibits breathing dining hypoxia in neonates. Respir Physiol 1997 110 251-260. [Pg.284]


See other pages where Hypoxia During Postnatal Development is mentioned: [Pg.264]    [Pg.264]    [Pg.261]    [Pg.625]    [Pg.242]    [Pg.266]    [Pg.279]   


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