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1 Departamento de Bioquimica y Biología Molecular y Fisiología/Instituto de Biología y Genética Molecular, Universidad de Valladolid/Consejo Superior de Investigaciones Científicas, Facultad de Medicina, 47005 Valladolid, Spain 2 Unidad de Cuidados Intensivos, Hospital Clínico Universitario de Valladolid, 47005 Valladolid, Spain
Hypoxia increases the release of neurotransmitters from chemoreceptor cells of the carotid body (CB) and the activity in the carotid sinus nerve (CSN) sensory fibers, elevating ventilatory drive. According to previous reports, perinatal hyperoxia causes CSN hypotrophy and varied diminishment of CB function and the hypoxic ventilatory response. The present study aimed to characterize the presumptive hyperoxic damage. Hyperoxic rats were born and reared for 28 days in 55%–60% O2; subsequent growth (to 3.5–4.5 months) was in a normal atmosphere. Hyperoxic and control rats (born and reared in a normal atmosphere) responded with a similar increase in ventilatory frequency to hypoxia and hypercapnia. In comparison with the controls, hyperoxic CBs showed (1) half the size, but comparable percentage area positive to tyrosine hydroxylase (chemoreceptor cells) in histological sections; (2) a twofold increase in dopamine (DA) concentration, but a 50% reduction in DA synthesis rate; (3) a 75% reduction in hypoxia-evoked DA release, but normal high [K+]0-evoked release; (4) a 75% reduction in the number of hypoxia-sensitive CSN fibers (although responding units displayed a nearly normal hypoxic response); and (5) a smaller percentage of chemoreceptor cells that increased [Ca2+]1 in hypoxia, although responses were within the normal range. We conclude that perinatal hyperoxia causes atrophy of the CB–CSN complex, resulting in a smaller number of chemoreceptor cells and fibers. Additionally, hyperoxia damages O2-sensing, but not exocytotic, machinery in most surviving chemoreceptor cells. Although hyperoxic CBs contain substantially smaller numbers of chemoreceptor cells/sensory fibers responsive to hypoxia they appear sufficient to evoke normal increases in ventilatory frequency.
(Received 17 June 2003;
accepted after revision 21 October 2003;
first published online 24 October 2003)
Corresponding author C. Gonzalez: Departamento de Bioquímica y, Biología Molecular y Fisiología, Facultad de Medicina, C/Ramón y Cajal no7, 47005 Valladolid, Spain. Email: constanc{at}ibgm.uva.es
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