Liu H, Wang S
Hua Xi Yi Ke Da Xue Xue Bao. 1993 Sep;24(3):241-5.
To investigate the mechanism of myocardial; tunning, a Langendorff model of rat hearts (n = 18) underwent 15 min ischemia with coronary flow at 0.2 ml/min and 10 min reperfusion with Ringer's solution of 1.06 mmol/L Mg2+. Histological exam revealed no myocardial necrosis. However, the recovery of pressure product (RPP) was only 77% compared with control period. The myocardial Ca2+ content and water content were significantly increased (P < 0.01, vs control hearts). Pretreatment with high concentration of Mg2+ (2.4 mmol/L) improved the recovery of postischemic ventricular function, attenuated the Ca2+ overload and myocardial edema. The results indicated that a brief period of low-flow ischemia could produce a postischemic ventricular dysfunction-the myocardial stunning. Calcium overload and myocardial edema might be two pathogenic factors. An increased Mg2+ had a protective effects on postischemic ventricular dysfunction, which may involve the following mechanisms: reduced Ca2+ overload and attenuated myocardial edema.
为研究心肌顿抑的机制，对18只大鼠心脏的Langendorff模型进行了实验，使其在冠状动脉血流为0.2 ml/min的条件下经历15分钟缺血，并在1.06 mmol/L Mg2+的林格氏液中再灌注10分钟。组织学检查未发现心肌坏死。然而，与对照期相比，压力乘积（RPP）的恢复仅为77%。心肌钙含量和水含量显著增加（P < 0.01，与对照心脏相比）。高浓度Mg2+（2.4 mmol/L）预处理可改善缺血后心室功能的恢复，减轻钙超载和心肌水肿。结果表明，短时间的低流量缺血可导致缺血后心室功能障碍——心肌顿抑。钙超载和心肌水肿可能是两个致病因素。镁离子增加对缺血后心室功能障碍具有保护作用，其机制可能如下：减少钙超载和减轻心肌水肿。
