Yoshiyama M, Ishikawa M, Miura I, Takeuchi K, Takeda T
First Department of Internal Medicine Osaka City University Medical School, Japan.
Jpn Circ J. 1994 Aug;58(8):662-70. doi: 10.1253/jcj.58.662.
Restoration of the ATP level after brief ischemia is limited by slow de novo ATP synthesis and substrate loss in a salvage pathways for ATP synthesis, and complete recovery requires several days in the stunned heart. Adenosine is a substrate for myocardial ATP synthesis. We measured myocardial ATP in both ex vivo and in vivo experiments by 31P magnetic resonance spectroscopy (31P-MRS) and investigated the time course of ATP content recovery after application of adenosine. Guinea-pig perfused hearts were subjected to 30 min of global ischemia and reperfused for 3 h with 50 microM adenosine. The ATP level increased from 54 +/- 5% to 117 +/- 4% of the pre-ischemic value (p < 0.01). In dogs, we occluded the left anterior descending coronary artery for 40 min to produce regional ischemia. Afterwards, we administered 100 mumol/h adenosine into the left ventricle for 2 h. ATP levels increased from 63 +/- 4% to 77 +/- 5% of the pre-ischemic value with adenosine (p < 0.05). However, ATP levels did not increase for a few hours after reperfusion both ex vivo and in vivo. Our 31P-MRS studies demonstrated that brief ischemia depressed ATP levels and that administration of adenosine accelerated ATP formation in post-ischemic hearts.
短暂缺血后ATP水平的恢复受到ATP从头合成缓慢以及ATP合成补救途径中底物损失的限制，在顿抑心脏中完全恢复需要数天时间。腺苷是心肌ATP合成的底物。我们通过31P磁共振波谱法（31P-MRS）在离体和体内实验中测量心肌ATP，并研究应用腺苷后ATP含量恢复的时间进程。豚鼠灌注心脏经历30分钟全心缺血，然后用50微摩尔/升腺苷再灌注3小时。ATP水平从缺血前值的54±5%增加到117±4%（p<0.01）。在犬类动物中，我们阻断左前降支冠状动脉40分钟以产生局部缺血。之后，我们以100微摩尔/小时的速度向左心室内注入腺苷2小时。使用腺苷后，ATP水平从缺血前值的63±4%增加到77±5%（p<0.05）。然而，在离体和体内再灌注后的几个小时内，ATP水平并未升高。我们的31P-MRS研究表明，短暂缺血会降低ATP水平，而应用腺苷可加速缺血后心脏中ATP的形成。
