English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/157932

Age protects from harmful effects produced by chronic intermittent hypoxia

AutorQuintero, M.; Olea, Elena ; Conde, Silvia V.; Obeso, Ana ; Gallego-Martin, Teresa ; González, Constancio ; Montserrat, Jose M.; Gómez-Niño, A.; Yubero, Sara ; Agapito, Teresa
Fecha de publicación2016
EditorJohn Wiley & Sons
CitaciónJournal of Physiology 594(6): 1773-1790 (2016)
ResumenObstructive sleep apnoea (OSA) affects an estimated 3-7% of the adult population, the frequency doubling at ages >60-65 years. As it evolves, OSA becomes frequently associated with cardiovascular, metabolic and neuropsychiatric pathologies defining OSA syndrome (OSAS). Exposing experimental animals to chronic intermittent hypoxia (CIH) can be used as a model of the recurrent hypoxic and O desaturation patterns observed in OSA patients. CIH is an important OSA event triggering associated pathologies; CIH induces carotid body (CB)-driven exaggerated sympathetic tone and overproduction of reactive oxygen species, related to the pathogenic mechanisms of associated pathologies observed in OSAS. Aiming to discover why OSAS is clinically less conspicuous in aged patients, the present study compares CIH effects in young (3-4 months) and aged (22-24 months) rats. To define potential distinctive patterns of these pathogenic mechanisms, mean arterial blood pressure as the final CIH outcome was measured. In young rats, CIH augmented CB sensory responses to hypoxia, decreased hypoxic ventilation and augmented sympathetic activity (plasma catecholamine levels and renal artery content and synthesis rate). An increased brainstem integration of CB sensory input as a trigger of sympathetic activity is suggested. CIH also caused an oxidative status decreasing aconitase/fumarase ratio and superoxide dismutase activity. In aged animals, CIH minimally affected CB responses, ventilation and sympathetic-related parameters leaving redox status unaltered. In young animals, CIH caused hypertension and in aged animals, whose baseline blood pressure was augmented, CIH did not augment it further. Plausible mechanisms of the differences and potential significance of these findings for the diagnosis and therapy of OSAS are discussed.
Identificadoresdoi: 10.1113/JP270878
e-issn: 1469-7793
issn: 0022-3751
Aparece en las colecciones: (IBGM) Artículos
Ficheros en este ítem:
Fichero Descripción Tamaño Formato  
accesoRestringido.pdf15,38 kBAdobe PDFVista previa
Mostrar el registro completo

Artículos relacionados:

NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.