Exposure to acute or chronic hypoxaemia in otherwise healthy humans results in compensatory increases in cerebral blood flow (CBF) at rest and during exercise referred to as hypoxic cerebral vasodilatation. These elevations in CBF offset the reduction in arterial oxygen content (CaO2 ) and maintain cerebral O2 delivery (CDO2 ) conforming to the conservation of mass principle. In this review, we discuss the fundamental principles that contribute to the defence of CDO2 and the corresponding implications for metabolism. We critically address to what extent the increase in CBF reflects an adaptive or indeed maladaptive physiological response. The molecular mechanisms of CBF regulation in hypoxia are also briefly discussed and future directions proposed. This article is protected by copyright. All rights reserved.
|Early online date||5 May 2016|
|Publication status||Published - 31 Aug 2016|
- hypoxic cerebral vasodilation
- cerebral blood flow