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Pflugers Arch ; 443(5-6): 858-65, 2002 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-11889586

RESUMEN

To determine whether prenatal hypoxia increases the risk of developing cardiovascular disorders as an adult and, if so, the identity of the cell mechanisms involved in such dysfunction, we evaluated the sympathoadrenal system and central areas related to cardiovascular events during development and the cardiovascular parameters in adults. Pregnant rats were exposed to hypoxia (10% oxygen) from embryonic day (E) 5 to E20 and the offspring studied at 1, 3, 9 and 12 weeks of age for neurochemistry and at 12 weeks of age for cardiovascular analysis. In the 1-, 3- and 9-week-old offspring, the levels and utilization of catecholamines were reduced in sympathetic ganglia, in target organs, in adrenals and in the rostral part of the A2 cell group in the nucleus tractus solitarius, but were increased in the locus coeruleus. In the 12-week-old adult offspring, the lowered autonomic nervous activity was restricted to cardiac-related structures, i.e. the stellate ganglion, heart and adrenals. In adult rats, prenatal hypoxia did not affect the cardiac parameters under resting conditions but increased blood pressure and the variability of blood pressure and heart rate under stress conditions. The altered metabolic activity of the sympathoadrenal system and related central areas during development and at adulthood for most structures might be part of the potential mechanisms contributing to cardiovascular disorders in adults.


Asunto(s)
Sistema Cardiovascular/embriología , Hipoxia/fisiopatología , Ganglio Estrellado/embriología , Glándulas Suprarrenales/metabolismo , Animales , Presión Sanguínea , Sistema Cardiovascular/metabolismo , Femenino , Frecuencia Cardíaca , Locus Coeruleus/embriología , Locus Coeruleus/metabolismo , Miocardio/metabolismo , Norepinefrina/metabolismo , Tamaño de los Órganos , Oxígeno/farmacología , Embarazo , Efectos Tardíos de la Exposición Prenatal , Ratas , Ratas Sprague-Dawley , Ganglio Estrellado/metabolismo , Estrés Fisiológico/fisiopatología
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