Jimenez E, del Nido P, Feinberg H, Levitsky S
Department of Surgery, New England Deaconess Hospital, Boston, Mass.
J Thorac Cardiovasc Surg. 1993 Jun;105(6):988-94.
Cytosolic calcium accumulation has been proposed as a mediator for the pathologic changes that occur during myocardial ischemia. Whether the rise in cytosolic calcium is a result of influx or redistribution from internal stores has not been elucidated. Isolated retroperfused rabbit hearts were subjected to ischemia at 37 degrees C. The distribution of calcium between cytosol and internal membrane stores and the relationship between cytosolic calcium and the onset of left ventricular contracture were investigated. One group of hearts was loaded with the fluorescent calcium probe Fura 2-AM to measure cytosolic calcium and a second group with chlortetracycline to indicate changes in membrane-bound calcium. After the onset of ischemia there is a rise in cytosolic calcium, at least in part attributable to redistribution of calcium from intraorganellar sites to cytosol. The release of membrane-bound calcium and rise in cytosolic calcium preceded the onset of irreversible ischemic injury, that is, contracture.
细胞溶质钙的蓄积已被认为是心肌缺血期间发生的病理变化的介质。细胞溶质钙的升高是由于钙内流还是从内部储存库重新分布所致,目前尚未阐明。将离体逆行灌注的兔心脏置于37℃进行缺血处理。研究了钙在细胞溶质和内膜储存库之间的分布以及细胞溶质钙与左心室挛缩发生之间的关系。一组心脏用荧光钙探针Fura 2-AM加载以测量细胞溶质钙,另一组用金霉素加载以指示膜结合钙的变化。缺血开始后,细胞溶质钙升高,至少部分归因于钙从细胞内位点重新分布到细胞溶质。膜结合钙的释放和细胞溶质钙的升高先于不可逆缺血损伤即挛缩的发生。