Benveniste H, Diemer N H
Institute of Neuropathology, University of Copenhagen, Denmark.
J Cereb Blood Flow Metab. 1988 Oct;8(5):713-9. doi: 10.1038/jcbfm.1988.118.
Several studies have found postischemic regional accumulation of calcium to be time-dependent and coincident with the progression of ischemic cell change. In the most vulnerable cells in the hippocampus one would therefore expect to find a primary and specific early uptake of calcium after ischemia. Autoradiograms of 45Ca and 3H-inulin distribution were investigated before and 1 h after 20 min ischemia in the rat hippocampus. Two different methodological approaches were used for administration of 45Ca: (a) administration via microdialysis probes, (b) intraventricular injection. During control conditions the 45Ca autoradiograms showed variations in distribution volume in accordance with 3H-inulin determination of extracellular space size. One hour after ischemia a massive accumulation of 45Ca was found in the dentate hilus. No change in the distribution pattern of 3H-inulin could be demonstrated 1 h after ischemia. We suggest that 45Ca accumulation in dentate hilus 1 h after ischemia is a result of increased Ca2+ uptake before irreversible cell damage occurs and is not due to passive influx of calcium across a leaky plasma membrane.
多项研究发现，缺血后钙在局部的蓄积具有时间依赖性，且与缺血性细胞变化的进展相一致。因此，在海马体中最易受损的细胞中，人们预期会发现缺血后钙的早期原发性特异性摄取。研究了大鼠海马体在缺血20分钟前及缺血后1小时的45Ca和3H-菊粉分布的放射自显影片。采用两种不同的方法给予45Ca：（a）通过微透析探针给药，（b）脑室内注射。在对照条件下，45Ca放射自显影片显示分布体积的变化与3H-菊粉测定的细胞外空间大小一致。缺血1小时后，在齿状回门发现大量45Ca蓄积。缺血1小时后，未发现3H-菊粉的分布模式有变化。我们认为，缺血1小时后齿状回门中45Ca的蓄积是在不可逆细胞损伤发生前Ca2+摄取增加的结果，而不是由于钙通过渗漏的质膜被动流入。
