Mechanisms of secondary injury (post-ischemic injury) in the central nervous system have cently 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 factars to the already ischemic neurophil.

Here we have designed experiment to investigate calcium paradox in astroglial cell line, humsn asttocytoma U1242MG. Intracellular calcium alterations in experimental cells were monitored by using calcium indicating dye fura-2 and epifluorescent photometry system.

Intracellular free calcium changes during reperfusion phase after exposure to low calcium led to a prampt increase in intracellular calcium level after 10 and 30 minutes. The way of calcium entry during the reperfusion phase was mediated by the revase mode of Na+/Ca(2+) 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 the same protocols.

A relatively small amount of intracellular calcium increase by the reverse mode of Na+/Ca(2+) exchanger during the reperfusion period is related to a limitation of enzyme activity and viability 24 hours later.