Korean J Anesthesiol.  1996 Apr;30(4):384-391. 10.4097/kjae.1996.30.4.384.

Reperfusion Injury in Glial Cells: The Phenomenon and Mechanism of "Calcium Paradox"

• Kim MH
• Lee BD
• Kim YH
• Shin BH

• KMID: 1860459
• DOI: http://doi.org/10.4097/kjae.1996.30.4.384

Abstract

BACKGROUND: 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.
METHODS
here we have designed experiment to investigate calcium paradox in astroglial cell line, human astrocytoma U1242MG. Intracellular calcium alterations in experimental cells were monitored by using calcium indicating dye fura-2 and epifluorescent photometry system.
RESULTS
Intracellular free calcium changes during reperfusion phase after exposure to low calcium led to a prompt increase in intracelluar 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 10uM increased cell viability. Also we observed an inverse relationship between major enzymatic activity in the astrocytoma cells(i.e., gultamine synthetase activity) and the duration of reperfusion in the the same protocols.
CONCLUSIONS
A relatively small amount of intracellular clcium increase by the reverse mode of Na+/Ca2+ exchanger during the reperfusion period is related to a limitation of enzyme activity and viability 24hours later.

Keyword

Brain; ischmia; cells; glia; viability; ions; calcium

MeSH Terms

Astrocytoma
Brain
Calcium
Cell Line
Cell Survival
Central Nervous System
Fura-2
Humans
Ions
Ligases
Neuroglia*
Neurons
Photometry
Reperfusion Injury*
Reperfusion*
Calcium
Fura-2
Ions
Ligases