Hoffmeister H M, Mauser M, Schaper W
Basic Res Cardiol. 1985 Jul-Aug;80(4):445-58. doi: 10.1007/BF01908189.
We investigated whether the postischemic acceleration of adenosine triphosphate (ATP) synthesis by means of precursor infusion is beneficial for the contractile function of reperfused myocardium. A coronary artery was occluded for 45 min in 21 dogs to produce a marked but reversible ischemia. During the following 3 hours of reperfusion either adenosine (n = 6) or AICAR (5-amino-imidazole-4-carboxamide-riboside) (n = 6) was infused intracoronarily by a small transfemoral catheter positioned in the LAD. ATP repletion by adenosine was nearly 50% of the deficit caused by the previous ischemia, the effect of AICAR on steady-state tissue ATP concentration was insignificant. Regional systolic function of these both groups was compared to that of a control group (n = 9) receiving only a saline infusion. We measured the regional function by subendocardially implanted ultrasound transducers using the transit time method. All three groups showed a reduction to about 25% of the initial segment shortening at the end of ischemia, followed by a quick recovery to half of the preocclusion segment shortening after reopening of the vessel. No further changes were observed in the control series during the 3 hours of reperfusion (50 +/- 10% SE segment shortening at the end). With adenosine infusion - in spite of the resulting considerable ATP elevation - no significant change of segmental contractile function occurred (44 +/- 5% SE segment shortening). Only the AICAR treated group differed from control. It produced a continuous deterioration during reflow resulting in a holosystolic bulging of -20% +/- 10% SE at the end of 3 hours of reperfusion. Our results show that there is no correlation between different ATP tissue levels achieved by adenosine infusion and systolic function in reperfused myocardium after regional reversible ischemia. We hypothesize that reperfusion dyskinesia is caused by a failure of energy utilisation rather than of energy supply.
我们研究了通过输注前体来加速缺血后三磷酸腺苷（ATP）合成是否对再灌注心肌的收缩功能有益。在21只犬中，将冠状动脉闭塞45分钟以产生明显但可逆的缺血。在随后3小时的再灌注期间，通过置于左前降支的小型经股导管冠状动脉内输注腺苷（n = 6）或AICAR（5-氨基-咪唑-4-甲酰胺-核苷）（n = 6）。腺苷使ATP补充量接近先前缺血所致ATP缺失量的50%，AICAR对稳态组织ATP浓度的影响不显著。将这两组的局部收缩功能与仅接受盐水输注的对照组（n = 9）进行比较。我们使用渡越时间法，通过心内膜下植入的超声换能器测量局部功能。所有三组在缺血结束时均显示节段缩短率降至初始值的约25%，血管重新开放后迅速恢复至闭塞前节段缩短率的一半。在对照组的3小时再灌注期间未观察到进一步变化（结束时节段缩短率为50±10%标准误）。输注腺苷时，尽管导致ATP显著升高，但节段收缩功能未发生显著变化（节段缩短率为44±5%标准误）。只有AICAR治疗组与对照组不同。在再灌注期间它出现持续恶化，在3小时再灌注结束时出现全收缩期膨出，膨出率为-20%±10%标准误。我们的结果表明，在局部可逆性缺血后再灌注的心肌中，通过输注腺苷所达到的不同ATP组织水平与收缩功能之间没有相关性。我们推测，再灌注运动障碍是由能量利用失败而非能量供应失败引起的。
