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Hypoxia of sleep apnoea: cardiopulmonary and cerebral changes after intermittent hypoxia in rats

Lookup NU author(s): Professor Raj KalariaORCiD, Dr John Fairlie, Arthur Oakley, Professor David Barer

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Abstract

Sleep apnoea (SA) is common, especially in elderly people. In severe cases, arterial P-O2 may be lowered for a third or more in a night of sleep. To simulate the degree and duration of severe SA we exposed rats in a normobaric environmental chamber to 10% O-2 for 4 h daily for 56 days (intermittent hypoxia: 1H group) and compared them with rats continuously exposed for 8 weeks (continuous hypoxia: CH group) and control rats breathing room air (normoxic: N group). We found significant cardiopulmonary and cerebral changes. Right ventricular hypertrophy developed in 1H and to a greater extent in CH. Small peripheral lung vessels developed thicker walls (assessed by a new method), which reduced their lumen, more in CH than 1H. Coronal brain sections were immunostained for the glucose-transporter 1 (GLUT1) and the vascular endothelial growth factor (VEGF). The percentages of immunoreactivity in the frontal and temporal cortex, hippocampus, accumbens and putamen were determined by image-capture analysis. We noted GLUT1 immunoreactivity of the capillaries was similarly increased in all regions after CH but less so after 1H. However, there was a significant linear trend in GLUT1 reactivity from N to 1H to CH (R-2 = 0.73, P = 0.007) that was also confirmed by analysis of variance. The extent of VEGF-stained neurones and glial cells was significantly increased in all regions after 1H but not after CH. This suggests that the signals for angiogenesis were complete or arrested after CH. Our findings have implications for the elderly subjected to hypoxic episodes during sleep apnoea. (C) 2004 Elsevier B.V. All rights reserved.

Publication metadata

Author(s): Kalaria RN, Spoors L, Laude EA, Emery CJ, Thwaites-Bee D, Fairlie J, Oakley AE, Barer DH, Barer GR

Publication type: Article

Publication status: Published

Journal: Respiratory Physiology & Neurobiology

Year: 2004

Volume: 140

Issue: 1

Pages: 53-62

ISSN (print): 1569-9048

ISSN (electronic): 1878-1519

Publisher: Elsevier BV

URL: http://dx.doi.org/10.1016/j.resp.2004.01.003

DOI: 10.1016/j.resp.2004.01.003

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