The Question of Uncoupling of Cerebral Oxidative Phosphorylation in Acute Cerebral Infarction
It is now well established that the autonomic nervous system plays an important role in control of the cerebral circulation (5). Information is now becoming available that neurotransmitters may exert important influences on cerebral metabolism. Certain neurotransmitters, such as norepinephrine and serotonin, cause a contractile response in the cerebral arteries when applied locally (14, 15). In both cerebral infarction and spinal cord injury, these neurotransmitters have been shown to accumulate in the damaged CNS tissue and hence in the cerebrospinal fluid (10, 11, 13, 18). It has been hypothesized from measurements of catecholamines in brain tissue that in addition to enhancing cerebral oxygen consumption, free norepinephrine in CNS tissues may also stimulate membrane-dependent processes such as oxidative phosphorylation and enzymatic disruption of lipids contained in neuronal membranes (1).
KeywordsCerebral Infarction Cerebral Metabolism Acute Cerebral Infarction Cerebral Oxygen Consumption Cerebral Infarc
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- 4.Hori, H., and Zervas, N. T.: “The effect of alpha-methyl-p-tyrosine on experimental stroke.” American Association of Neurological Surgeons Scientific Program, 1973, Los Angeles, Paper #30.Google Scholar
- 12.Osterholm, J. L., and Mathews, G. J.: “Altered norepinephrine metabolism following experimental spinal cord injury. II. Protection against traumatic spinal cord hemorrhagic necrosis by norepinephrine synthesis blockade with alpha-methyl-tyrosine.” J. Neurosurg. 36:395 (1972).PubMedCrossRefGoogle Scholar
- 17.Siesjö, B. K., and Plum, F.: “Pathophysiology of anoxic brain damage.” In Biology of Brain Dysfunction, G. E. Gaull, ed. Vol. 1, New York-London: Plenum Press (1973), pp. 319–372.Google Scholar