Cerebral Circulation in REM Sleep: Is Oxygen a Main Regulating Factor?
P. Lenzi1, G. Zoccoli1, A.M. Walker2, C. Franzini1.
1Department of Human and General Physiology, University of Bologna, Bologna, Italy
2Institute of Reproduction and Development, Monash University, Clayton, Victoria, Australia
In the transition from NREM to REM sleep, as in other instances of brain activation, a marked
increase in cerebral blood flow and glucose uptake is observed, together with a lesser increase in
O2 uptake. Brain activation also entails an increase in capillary PO2 and lactate
production. The hypothesis of saturation of the oxidative machinery was advanced to explain
anaerobic glycolysis and lactate production in the presence of high PO2, but data are available
that cannot be explained by this hypothesis: hypoxic spots exist in the brain, augmenting in arterial hypoxia
and disappearing in arterial hyperoxia, while tissue [H+] lowers as arterial PO2
increases beyond 100 mmHg. Additional hypotheses are thus required. We suggest that
O2 diffusion limitation exists in the brain: microregions lying at mid-distance between
capillaries may become hypoxic and partly resort to anaerobic glycolysis. These microregions are thought
to enlarge with increasing metabolic rate or arterial hypoxia and give rise to vasodilatatory signals
regulating local blood flow. REM sleep time is strongly reduced by hypoxic and increased by hyperoxic
atmosphere, in accordance with the existence of an O2 diffusion limitation. Any pathological
decrease in arterial PO2 and/or O2 delivery creates a specific risk in REM
sleep.