Rappaport Z H, Young W, Flamm E S
Stroke. 1987 Jul-Aug;18(4):760-4. doi: 10.1161/01.str.18.4.760.
Entry of Ca ions into ischemic neurons is believed to cause cell damage. Although several investigators have demonstrated changes in extracellular Ca ionic activity consistent with Ca movement into cells, direct and quantitative evidence for Ca entry into ischemic cells is lacking. We used atomic absorption spectroscopy to measure the regional distribution of tissue Ca contents of rat brains sampled at 2, 4, and 24 hours after middle cerebral artery occlusion (MCAo). At 4 hours after MCAo, Ca concentrations increased significantly (p less than 0.005) in the ischemic middle cerebral artery territory, i.e., the pyriform and frontoparietal cortices, but not in the surrounding brain. At 24 hours, Ca concentrations in the pyriform and frontoparietal cortex were respectively 30.79 (+/- 2.90) and 29.19 (+/- 3.28) mumol/g dry tissue wt compared with 11.9 (+/- 1.7) mumol/g in sham-occluded rats. Tissue Ca concentration changes in the parasagittal cortex and basal ganglia adjacent to the infarct site were much smaller and did not differ significantly from controls until 24 hours. In the ischemic middle cerebral artery territory, greater than 1.0 mumoles of Ca entered per gram of dry tissue weight per hour during the first 4 hours after MCAo. Linear regression analysis revealed a significant correlation (r = 0.9722) between changes in tissue Ca and water, with a slope indicating that 5.88 mumoles of Ca accompanied each milliliter of water entering the lesioned hemisphere. Such massive accumulations of Ca not only confirm Ca entry into injured cells, but indicate the presence of a remarkable Ca sink which sequestered within 24 hours more than 17 times the amount of free Ca present in the tissue before MCAo.
