Energy-requiring cell functions in the ischemic brain

Their critical supply and possible inhibition in protective therapy

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✓ The energy-requiring cell functions in the brain are described. The role of specific inhibition of these functions, and their critical low-supply levels of blood flow and oxygen are reviewed in relation to clinical management of focal and complete global cerebral ischemia.

Article Information

Address reprint requests to: Jens Astrup, M.D., Department of Neurosurgery 433, Hvidovre Hospital, 2650 Hvidovre, Denmark.

© AANS, except where prohibited by US copyright law.

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Figures

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    Total cerebral metabolic rate (CMR) and energy-requiring cell functions in the brain. The amount of energy consumed by synaptic transmission and associated Na+-K+ transport varies according to the functional state of the brain. This consumption can be completely inhibited by barbiturates given in large doses. The residual portion of energy consumption is indicated as 100% on the scale. It consists of two parts, one of which is consumed by membrane leakages and associated Na+-K+ “back”-transport, and can be inhibited by lidocaine and ouabain (40% to 50%), while the remaining part is shared by a number of other processes (see text) of which no specific mode of inhibition has yet been found.

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    The zone of penumbra in the baboon with middle cerebral artery occlusion. In the acute state, the central black area has flows below the threshold of membrane failure, as indicated by a high extracellular potassium concentration. In the chronic state, this area corresponds to the infarcted area. The surrounding zone of penumbra (dotted area) has flows between the threshold levels of synaptic transmission failure and membrane failure. In the acute state this area appears functionally inactivated, but in the chronic state it appears viable without signs of infarction. (Diagram after Symon and colleagues.11,21,22,120–122)

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