Osmotic opening of the blood‐brain barrier and local cerebral glucose utilization

Abstract

The effects of osmotic opening of the blood-brain barrier (BBB) on local cerebral glucose utilization (LCGU) were studied in rats with the carbon 14-deoxyglucose method. The BBB was opened to Evans blue dye by unilateral carotid artery perfusion with hypertonic mannitol solution. (14C)-Deoxyglucose was injected 15 minutes or two to three hours later. Osmotic opening of the BBB resulted in focal areas of intense LCGU in affected areas of the perfused hemisphere. In the contralateral hemisphere, glucose utilization was diminished, especially in cerebral cortical areas. The effects were reversible. LCGU was normal in both hemispheres when permeability to Evans blue returned to normal two to three hours after carotid artery perfusion. In 3 of 5 experiments the administration of high doses of intravenous diazepam immediately following carotid artery perfusion with mannitol prevented an increase in LCGU in the perfused hemisphere but did not prevent lowering of LCGU in the contralateral hemisphere. Increased LCGU following osmotic opening of the BBB was not accompanied by a rise in local cerebral blood flow as measured by the iodoantipyrine method. Blood flow was, in fact, significantly decreased.

The Effects of Serotonin on Local Cerebral Blood Flow

“…Pappius et al (1979) found decreases in cerebral blood flow on the order of 25-65% fol lowing BBB disruption. The obvious quantitative difference between their data and our own may partly be due to the considerably greater rate of infusion (2.49 ml 1.4 M mannitol in 30 s) used by these investigators.…”

Localization of Functional Activity in the Central Nervous System by Measurement of Glucose Utilization with Radioactive Deoxyglucose

“…Unilateral opening of the blood-brain barrier in rats by unilat eral carotid injection with a hyperosmotic mannitol solution leads to widely distributed discrete regions of intensely increased glucose utilization in the ip silateral hemisphere (Pappius et al , 1979). These focal regions of hypermetabolism may reflect local regions of seizure activity.…”

Bilirubin-Induced Changes in Brain Energy Metabolism after Osmotic Opening of the Blood-Brain Barrier

“…This pattern of disturbance is indicative of either severe ischemia or mitochondrial dysfunction involving a block in NADH transport or utilization (32). Osmotic opening of the blood-brain barrier is accompanied by an initial increase in cerebral blood flow lasting up to 6 min (33), followed by a decrease in flow associated with a mild vasogenic brain edema lasting up to I h (34,35). During this time there is uncoupling of cerebral blood flow and metabolism.…”