Hultman J, Ronquist G, Forsberg J O, Hansson H E
Eur Surg Res. 1983;15(4):200-7. doi: 10.1159/000128354.
The myocardial energy restoration of ischemic damage by administration of phosphoenolpyruvate during reperfusion was investigated in a paracorporeal heart model modified in the rat. Excised hearts were subjected to 15 min of complete global ischemia at ischemia at 37 degrees C before pulsatile blood reperfusion for 30 min. One group (n = 7) was supplemented with 67 mumol of phosphoenolpyruvate and 0.67 mumol of adenosine triphosphate dissolved in 10 ml of saline and another with plain saline (nonsupplemented) during reperfusion. All hearts were freeze-clamped after 30 min of reperfusion and subjected to energy content analysis. The adenylate charge potential was 0.91 +/- 0.01 (mean +/- SD) for the supplemented and 0.85 +/- 0.06 (mean +/- SD) for the nonsupplemented group. This difference was significant (p less than 0.02). Concomitantly the outflow of creatine kinase was less for the supplemented group. The translocation of phosphoenolpyruvate into the myocardial cells seems possible by blood supplementation of a lower dose of adenosine triphosphate.
在一种改良的大鼠体外心脏模型中，研究了在再灌注期间给予磷酸烯醇丙酮酸对缺血性损伤心肌能量恢复的影响。将离体心脏在37℃下进行15分钟的完全全心缺血，然后进行30分钟的搏动性血液再灌注。一组（n = 7）在再灌注期间补充溶解于10毫升生理盐水中的67微摩尔磷酸烯醇丙酮酸和0.67微摩尔三磷酸腺苷，另一组在再灌注期间补充生理盐水（未补充）。再灌注30分钟后，所有心脏均进行冷冻钳夹并进行能量含量分析。补充组的腺苷酸荷电位为0.91±0.01（平均值±标准差），未补充组为0.85±0.06（平均值±标准差）。这种差异具有显著性（p＜0.02）。同时，补充组肌酸激酶的流出量较少。通过补充较低剂量的三磷酸腺苷，磷酸烯醇丙酮酸似乎有可能转运到心肌细胞中。
