Vial C, Owen P, Opie L H, Posel D
J Mol Cell Cardiol. 1987 Feb;19(2):187-97. doi: 10.1016/s0022-2828(87)80561-8.
The status of ATP as a possible coronary vasodilator remains poorly understood. The onset of hypoxia induced a rapid and transient increase of the ATP concentration in the coronary effluent of the isolated perfused rat heart from 0.8 +/- 0.2 nM to the average peak value of 1.3 +/- 0.2 nM (P less than 0.01) at 2 +/- 0.5 min; at the same time the coronary flow increased 2-fold so that the rate of ATP release increased from 10.2 +/- 2.9 to 21.4 +/- 4.2 pmol/g/min (P less than 0.005). Hypoxia also produced a peak rate release of adenosine of 93 +/- 5 nM/g/min occurring only after the peak increase of coronary flow and also after the peak release of ATP; at peak coronary flow, however, the adenosine concentration was sufficient for vasodilation (0.31 +/- 0.19 microM). Peak release of ATP and of adenosine preceded that of lactate dehydrogenase. 10(-6) M adrenaline induced a rapid increase of coronary flow and release of ATP, the concentration of which rose from 0.9 +/- 0.3 nM to an average peak of 1.7 +/- 0.2 nM (P less than 0.01) at 2 +/- 0.3 min. The rate of increase of ATP in the coronary effluent paralleled the rate of early rise of coronary flow, yet adenosine had also risen to vasodilatory values (0.28 +/- 0.5 microM). The absolute changes in the measured concentrations of ATP in the coronary effluent were more variable and 1000 X less in concentration than those of adenosine. Hence coronary dilation could be explained by adenosine without involving ATP, although an additional vasodilatory role for ATP could not be excluded, especially in the early phases of vasodilation. In one condition, hypoxic K-arrested hearts, the increase in coronary flow could not be linked to release of either adenosine or ATP. The changes in concentrations of potential vasodilators measured in the coronary effluent do not necessarily reflect changes in the interstitial fluid.
ATP作为一种可能的冠状动脉血管扩张剂，其状况仍未得到充分了解。缺氧开始后，在2±0.5分钟时，离体灌注大鼠心脏冠脉流出液中的ATP浓度从0.8±0.2 nM迅速短暂升高至平均峰值1.3±0.2 nM（P<0.01）；与此同时，冠脉血流量增加了2倍，使得ATP释放速率从10.2±2.9增加到21.4±4.2 pmol/g/min（P<0.005）。缺氧还导致腺苷的峰值释放速率为93±5 nM/g/min，仅在冠脉血流量峰值增加之后以及ATP峰值释放之后出现；然而，在冠脉血流量峰值时，腺苷浓度足以引起血管舒张（0.31±0.19 μM）。ATP和腺苷的峰值释放先于乳酸脱氢酶。10⁻⁶ M肾上腺素引起冠脉血流量迅速增加和ATP释放，其浓度在2±0.3分钟时从0.9±0.3 nM升至平均峰值1.7±0.2 nM（P<0.01）。冠脉流出液中ATP的增加速率与冠脉血流量早期上升速率平行，但腺苷也已升至血管舒张值（0.28±0.5 μM）。冠脉流出液中测得的ATP浓度的绝对变化更具变异性，且浓度比腺苷低1000倍。因此，冠脉舒张可以用腺苷来解释而不涉及ATP，尽管不能排除ATP的额外血管舒张作用，尤其是在血管舒张的早期阶段。在一种情况下，即缺氧钾停跳心脏，冠脉血流量的增加与腺苷或ATP的释放均无关联。在冠脉流出液中测得的潜在血管扩张剂浓度的变化不一定反映组织间液中的变化。
