Lessons from the laboratory; integrated regulation of cerebral blood flow during hypoxia.

Abstract

What is the topic of this review? What is the mechanism underlying the control of human cerebral blood flow in hypoxia and what are the consequences? What advances does it highlight? Although appropriate elevations in cerebral blood flow occur in acute and chronic hypoxia, neuronal processes are more sensitive to even small hypoxic insults; hence, they can result in maladaptive consequences despite maintenance of global oxygen delivery. 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 and maintain cerebral O2 delivery, conforming to the conservation of mass principle. In this review, we discuss the fundamental principles that contribute to the defence of cerebral O2 delivery 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.