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KMID : 0356919960300030370
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Korean Journal of Anesthesiology
1996 Volume.30 No. 3 p.370 ~ p.372
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Letters to Editor
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Abstract
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Background:
@EN Mechanisms of secondary injury (post-ischemic injury) in the central nervous system have recently reported in a vast of amount of experiments. Among many factors which give rise to post-ischemic neuronal damage, glial deterioration probably
mediated
by calcium paradox, could be another of the aggravating deleterious factors to the already ischemic neurophil.
@ES Methods:
@EN Here we have designed experiment to investigate calcium paradox in astroglial cell line, human astrocytoma U124MG. Intracellular calcium alterations in experimental cells were monitored by using calcium indicating dye fura-2 and
epifluorescent
photometry system.
@ES Results:
@EN Intracellular free calcium changes during reperfusion phase after exposure to lo calcium led to a prompt increase in intracellular calcium level after 10 and 30 minutes. The way of calcium entry during the reperfusion phase was mediated by
the
reverse mode of Na+/Ca2+ exchanger. Cells that had a reduction of reperfusate calcium to 10 uM increased cell viability. Also we observed an inverse relationship between major enzymatic activity in the astrocytoma cells (I.e., glutamine
synthetase
activity) and the duration of reperfusion in the same protocols.
@ES Conclusions;
@EN A relatively small amount of intracellular calcium increase by the reverse mode of Na+/Ca2+ exchanger during the reperfusion period I related to a limitation of enzyme activity and viability 24 hours later (Korean J Anesthesiol 1996; 30:
384~391)
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