RT info:eu-repo/semantics/article
T1 Age protects from harmful effects produced by chronic intermittent hypoxia
A1 Quintero Coca, Miguel
A1 Olea Fraile, Elena
A1 Conde, Silvia V.
A1 Gallego Martín, Teresa
A1 González, C.
A1 González, Constancio
A1 Montserrat, Josep M.
A1 Gómez Niño, María Ángeles
A1 Yubero Benito, Sara
A1 Agapito Serrano, María Teresa
K1 Intermittent hypoxia
K1 Hipoxia intermitente
K1 Sleep apnoea
K1 Apnea del sueño
AB Obstructive 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 O2 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.
PB The Physiological Society
SN 1469-7793
YR 2016
FD 2016
LK https://uvadoc.uva.es/handle/10324/46963
UL https://uvadoc.uva.es/handle/10324/46963
LA eng
NO The Journal of Physiology, 2016, vol. 594, n. 6. p. 1773–1790
NO Producción Científica
DS UVaDOC
RD 26-abr-2024