PMID: 2484187Dec 1, 1989Paper

Monoamine metabolism after transient global ischemia. Mechanism of delayed postischemic hypoperfusion

Neurologia Medico-chirurgica
C Maruki

Abstract

During the period of recirculation following transient global ischemia, an initial hyperemia is succeeded by a secondary decrease in cerebral blood flow, termed "delayed postischemic hypoperfusion." It has been suggested that this phenomenon can lead to additional brain damage after the initial ischemic insult. One proposed mechanism of delayed postischemic hypoperfusion is increased cerebrovascular smooth muscle tone. Release of vasoactive amines, formation of vasoactive products of arachidonic acid metabolism, and disturbance of calcium ion homeostasis in cerebrovascular smooth muscle may contribute to postischemic vasoconstriction. In this study, monoamine metabolism following transient global ischemia was investigate. Mongolian gerbils subjected to 15 minutes of temporal bilateral common carotid artery occlusion and up to 6 hours of recirculation were employed as a model of transient global ischemia. In this model, secondary energy failure reportedly occurs after 6 hours of recirculation. Regional cerebral concentrations of monoamines and their metabolites were determined by high-performance liquid chromatography with electrochemical detection. After 4 to 6 hours of recirculation, accumulation of vasoactive amine, 5-hydroxy...Continue Reading

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