Daenen W, Flameng W
Angiology. 1981 Aug;32(8):543-51. doi: 10.1177/000331978103200804.
The cardioprotective effects of lidoflazine, a drug with calcium homeostatic properties, were studied in 12 dogs (6 drug-treated and 6 controls) subjected to 1-hour normothermic global ischemia. None of the control dogs could be weaned from the extracorporeal bypass after 30 minutes of reperfusion. In contrast, all acutely pre-treated animals were able to support their own circulation. Recovery of pre-ischemic values in this group was 97 +/- 3% for systolic aortic pressure, 69 +/- 7% for diastolic aortic pressure, 97 +/- 10% for left ventricular pressure, and 84 +/- 11% for cardiac output. Electron microscopy and calcium cytochemistry were done on left ventricular biopsies taken before, during, and after ischemic arrest. In the control group, severe damage to the sarcolemma and the mitochondria was found at the end of the ischemic period and became more prominent after 5 and 30 minutes of reperfusion. There was great accumulation of calcium in the damaged mitochondria. In the lidoflazine-treated dogs, these lesions were largely prevented. These findings suggest a strong cardioprotective effect of lidoflazine during severe myocardial ischemia.
利多氟嗪是一种具有钙稳态特性的药物,研究了其对12只犬(6只药物治疗组和6只对照组)进行1小时常温全心缺血的心脏保护作用。在再灌注30分钟后,对照组犬无一能够脱离体外循环。相比之下,所有急性预处理动物都能够维持自身循环。该组缺血前值的恢复情况为:主动脉收缩压97±3%,主动脉舒张压69±7%,左心室压力97±10%,心输出量84±11%。在缺血停搏前、期间和之后,对左心室活检组织进行了电子显微镜检查和钙细胞化学分析。在对照组中,缺血期末发现肌膜和线粒体严重受损,再灌注5分钟和30分钟后更为明显。受损线粒体中有大量钙蓄积。在利多氟嗪治疗的犬中,这些损伤在很大程度上得到了预防。这些发现表明利多氟嗪在严重心肌缺血期间具有强大的心脏保护作用。