Cerebral blood flow and glucose utilization following opening of the blood-brain barrier and during maturation of the rat brain.
This paper reviews that relation between regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) under normal conditions of altered functional activity, following disruption of the blood-brain barrier by osmotic stress or hypertension, and during development and maturation of the rat brain. rCBF usually increases in parallel with LCGU when neuronal activity in the central nervous system increases. However, disruption of the blood-brain barrier disturbs this coupling between rCBF and LCGU. the blood-brain barrier, which is located at the continuous cerebrovascular endothelium, protects against brain edema and helps to maintain normal cerebral metabolism. When the barrier is disrupted by osmotic stress or by hypertension, LCGU increases markedly, due to increased neuronal activity, and brain edema develops. rCBF does not increase, however, possibly because brain edema prevents cerebral vasodilatation. rCBF and LCGU follow separate time courses during development and maturation of the rat brain. Both parameters increase between the ages of 1 and 3 months, but rCBF continues to rise from 3 to 12 months when LCGU simultaneously falls. The divergent time courses of these two parameters of brain functional activity may reflect an age-related change in the sensitivity of the cerebrovascular bed to metabolic factors that regulate rCBF.
D000375:Aging; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000254:growth & development* / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology; D002560:Cerebrovascular Circulation; D005947:Glucose / Q000378:metabolism*; D009994:Osmolar Concentration; D009997:Osmotic Pressure; D051381:Rats; D012039:Regional Blood Flow
D005947:Glucose