A functional disturbance contributing to the growth of the infarct core into the penumbra zone is the generation of peri-infarct spreading depressionlike depolarizations. These depolarizations are initiated at the border of the infarct core and spread over the entire ipsilateral hemisphere. During spreading depression the metabolic rate of the tissue markedly increases in response to the greatly enhanced energy demands of the activated ion-exchange pumps. In the healthy brain the associated increase of glucose and oxygen demands is coupled to a parallel increase of blood flow but in the peri-infarct penumbra this flow response is suppressed or even reversed . As a result, a misrelationship arises between the increased metabolic workload and the low oxygen supply, leading to transient episodes of hypoxia and the stepwise increase in lactate during the passage of each depolarization.
The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the linear relationship between the number of depolarizations and infarct volume. Correlation analysis of this relationship suggests that during the initial 3 hours of vascular occlusion each depolarization increases the infarct volume by more than 20%. This is probably one of the reasons that glutamate antagonists reduce the volume of brain infarcts because these drugs are potent inhibitors of spreading depression.
Peri-infarct spreading depressions are depolarizations initiated at the border of the infarct core and may contribute to progression of ischemic injury.
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