Abstract
The brain is critically dependent on a continuous supply of oxygen and glucose. Neuronal function depends almost exclusively on oxidative glucose metabolism and the brain has only limited stores of energy-generating substrates. Reduction of cerebral blood flow below a threshold required for maintaining the integrity compartment of the brain’s metabolism results in cerebral ischaemia, the major cause of metabolic brain injury. Cerebral ischaemia can be global or focal, which differ in cause, pathophysiology, localization, and to a certain extent in treatment strategies. Decreased global cerebral blood flow below ischaemic thresholds due to hypotension or insufficient cardiac output usually compromises the entire brain. In animal models of global cerebral ischaemia damage is most likely to occur first in certain vulnerable regions including the pyramidal cells of the CA1 region of the hippocampus (limbic system), Purkinje cells (cerebellum), and layers 3, 5, and 6 of the cortex. This pattern of selective vulnerable neurons has also been observed in humans, and may account for the poor neurologic outcome of survivors of cardiac arrest [1].
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Illievich, U.M., Machata, AM., Spiss, C.K. (2002). Brain Protection. In: Gullo, A. (eds) Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2099-3_3
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DOI: https://doi.org/10.1007/978-88-470-2099-3_3
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