Darsinos J, Karli J, Pistevos A, Levis G, Moulopoulos S
Department of Medicine, University of Athens, Greece.
Angiology. 1988 Oct;39(10):865-72. doi: 10.1177/000331978803901003.
To evaluate the effect of hypocalcemia on myocardial creatine kinase (CK) depletion after brief coronary artery occlusion and reperfusion, dogs were rendered hypocalcemic via systemic hemodialysis for eighty minutes in the absence of Ca. Control animals were hemodialysed in the presence of Ca. The left anterior descending coronary artery was then occluded for six minutes and reperfusion for eighty minutes occurred at low flow of dialysate. A 50% decrease in serum Ca of the hypocalcemic animals during the eighty minutes of hemodialysis resulted in a significant (about 35%) decrease of myocardial Ca. Comparison of the myocardial creatine kinase activity following reperfusion showed preservation of the enzyme in the ischemic areas of the hypocalcemic animals, whereas the CK activities of the ischemic areas of the normocalcemic animals were much lower (p less than 0.005). During the reperfusion period serum Ca of the hypocalcemic group increased to 75% of that of the normocalcemic group while myocardial Ca of both ischemic and nonischemic areas reequilibrated to normocalcemic values. Hemodynamic parameters during the various phases of the experiment were not altered significantly. It is concluded that transient decrease of myocardial Ca produced by hypocalcemia prior to occlusion leads to protection against myocardial damage after brief coronary ligation.
为评估低钙血症对短暂冠状动脉闭塞和再灌注后心肌肌酸激酶（CK）消耗的影响，在无钙情况下通过全身血液透析使犬低钙血症80分钟。对照动物在有钙的情况下进行血液透析。然后闭塞左冠状动脉前降支6分钟，并在低流量透析液情况下再灌注80分钟。低钙血症动物在80分钟血液透析期间血清钙降低50%，导致心肌钙显著降低（约35%）。再灌注后心肌肌酸激酶活性比较显示，低钙血症动物缺血区域的该酶得以保留，而正常钙血症动物缺血区域的CK活性则低得多（p<0.005）。在再灌注期间，低钙血症组的血清钙升至正常钙血症组的75%，而缺血和非缺血区域的心肌钙均重新平衡至正常钙血症值。实验各阶段的血流动力学参数无显著改变。结论是，闭塞前低钙血症导致的心肌钙短暂降低可保护心脏免受短暂冠状动脉结扎后的心肌损伤。
