Zografos P, Watts J A
Department of Biology, University of North Carolina, Charlotte 28223.
Am J Cardiovasc Pathol. 1990;3(2):155-65.
Effects of diltiazem upon mitochondrial ultrastructure and distribution of calcium were studied following ischemia (27 minutes) and reperfusion (30 minutes). Hearts receiving no drug recovered low contractile function, while mitochondria nearly doubled in cross-sectional area (0.98 vs 0.56 micron 2) and were structurally damaged (1.88 vs 0.17 score). Mitochondria contained fine calcium deposits (0.029-micron diam) in mildly damaged cells, larger deposits in moderately damaged cells, and a large deposit (0.17-0.29-micron diam) in severely injured cells. Glycocalyx Ca2+ stain, observed in nonischemic hearts, was reduced in moderately and severely damaged cells. Increased mitochondrial Ca2+ may be associated with loss of glycocalyx Ca2+. Diltiazem (7.5 microns), added before ischemia, improved recovery of contractile function and prevented mitochondrial swelling, structural grade change, and increase in mitochondrial Ca2+. Reduction in mitochondrial Ca2+ stain by diltiazem was associated with the maintenance of normal glycocalyx Ca2+.
研究了地尔硫䓬对缺血（27分钟）及再灌注（30分钟）后线粒体超微结构和钙分布的影响。未用药的心脏收缩功能恢复较差，而线粒体横截面积几乎翻倍（0.98对0.56平方微米）且结构受损（评分1.88对0.17）。线粒体在轻度受损细胞中含有细小的钙沉积（直径0.029微米），在中度受损细胞中含有较大的沉积，在严重受损细胞中含有大的沉积（直径0.17 - 0.29微米）。在非缺血心脏中观察到的糖萼钙染色，在中度和重度受损细胞中减少。线粒体钙增加可能与糖萼钙丢失有关。在缺血前加入地尔硫䓬（7.5微米）可改善收缩功能恢复，并防止线粒体肿胀、结构分级变化以及线粒体钙增加。地尔硫䓬使线粒体钙染色减少与糖萼钙的正常维持有关。
