首页 | 本学科首页   官方微博 | 高级检索  
     


Age protects from harmful effects produced by chronic intermittent hypoxia
Authors:M. Quintero  E. Olea  S. V. Conde  A. Obeso  T. Gallego‐Martin  C. Gonzalez  J. M. Monserrat  A. Gómez‐Ni?o  S. Yubero  T. Agapito
Abstract: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.

Abbreviations

24M
rats aged 22–24 months
24MCIH
rats aged 22–24 months exposed to chronic intermittent hypoxia
3M
rats aged 3–4 months
3MCIH
rats aged 3–4 months exposed to chronic intermittent hypoxia
A
adrenaline
AP
arterial pressure
CA
catecholamine
CB
carotid body
CI
confidence interval
CIH
chronic intermittent hypoxia
CRP
C‐reactive protein
CuZnSOD
cytoplasmic superoxide dismutase
DA
dopamine
EGSH
glutathione redox potential
GPx
glutathione peroxidase
GSH
reduced glutathione
GSSG
oxidized glutathione
LPO
lipid peroxide
MnSOD
mitochondrial superoxide dismutase
MV
minute ventilation
NA
noradrenaline
NTS
nucleus of the tractus solitarius
OSA
obstructive sleep apnoea
OSAS
obstructive sleep apnoea syndrome
PaO2
arterial oxygen pressure
RA
renal artery
ROS
reactive oxygen species
RVLM
rostroventrolateral medulla
SaO2
arterial haemoglobin saturation
SOD
superoxide dismutase
SSA
5‐sulfosalicylic acid
TV
tidal volume
UA
upper airway
Keywords:
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号