Mochizuki Y, Yata Y, Miyamoto H, Sasaki T, Horikoshi S, Arai T
Rinsho Kyobu Geka. 1989 Apr;9(2):176-9.
The potential for enhancing myocardial protection by adding ATP to cardioplegic solution was investigated in a rat heart model of cardiopulmonary bypass. Concentration of added ATP was 0.01 mM and 0.1 mM. The hearts were perfused by working heart model for 10 min as a baseline hemodynamic variables and they underwent infusion of cardioplegic solution followed by 20 min cardiac arrest with myocardial temperature at 37 degrees C. The ATP added group revealed good % recovery of aortic flow after 20 min period of ischemic arrest compared to the ATP free control group. But there is no difference between 0.01 mM and 0.1 mM ATP added group. ATP added group showed higher ATP concentration in myocardium and ATP/ADP and energy charge after 20 min of ischemic arrest than ATP free control group. But total adenosine showed no difference. The result suggested that ATP was a protective myocardial agent in cardioplegic solutions and ATP might protect membrane-bound ATP dependent process by ensuring energy supply.
在大鼠体外循环心脏模型中,研究了在心脏停搏液中添加三磷酸腺苷(ATP)增强心肌保护的可能性。添加的ATP浓度为0.01 mM和0.1 mM。心脏通过工作心脏模型灌注10分钟作为基线血流动力学变量,然后输注心脏停搏液,随后在心肌温度为37摄氏度的情况下心脏停搏20分钟。与无ATP的对照组相比,添加ATP的组在缺血性停搏20分钟后显示出较好的主动脉血流恢复百分比。但添加0.01 mM和0.1 mM ATP的组之间没有差异。添加ATP的组在缺血性停搏20分钟后心肌中的ATP浓度、ATP/ADP和能量电荷高于无ATP的对照组。但总腺苷没有差异。结果表明,ATP是心脏停搏液中的一种心肌保护剂,ATP可能通过确保能量供应来保护膜结合的ATP依赖性过程。