Gambassi G, Capogrossi M C
Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD.
Cardiologia. 1992 Aug;37(8):587-9.
Myocardial acidosis, as during ischemia, profoundly modifies excitation-contraction mechanisms. The decreased myofilament sensitivity to Ca2+ reduces contractility regardless of an intracellular accumulation of Ca2+. To determine the source for this increase in Ca2+ we evaluated the effect of acidosis on diastolic [Ca2+] and mitochondrial [Ca2+]. We used single cardiac cells loaded with the fluorescent probes, indo-1 for Ca2+ and SNARF-1 for pH. Acidosis increases [Ca2+] both in cytosol and mitochondria. The cytosolic accumulation depends, most likely, on an active release from mitochondria. A competition among Ca2+ and H+ ions may, instead, explains the increase in mitochondrial [Ca2+].
心肌酸中毒，如在缺血期间，会深刻改变兴奋 - 收缩机制。肌丝对Ca2+的敏感性降低会降低收缩性，而与细胞内Ca2+的积累无关。为了确定这种Ca2+增加的来源，我们评估了酸中毒对舒张期[Ca2+]和线粒体[Ca2+]的影响。我们使用装载了荧光探针的单个心肌细胞，用indo - 1检测Ca2+，用SNARF - 1检测pH。酸中毒会使细胞质和线粒体中的[Ca2+]增加。细胞质中的积累很可能依赖于线粒体的主动释放。相反，Ca2+和H+离子之间的竞争可能解释了线粒体[Ca2+]的增加。
