Bernauer W
Department of Pharmacology, University of Freiburg, FRG.
Basic Res Cardiol. 1991 Jan-Feb;86(1):1-10. doi: 10.1007/BF02193866.
In isolated perfused rat hearts global ischemia for 2, 5, and 15 min was produced. Depending on the duration of the ischemia, postischemic reperfusion led to the release of adenosine and its catabolites, and to more or less severe ventricular tachyarrhythmias. When ventricular fibrillation occurred, a highly significant increase in the purine release was observed compared with non-fibrillating hearts. Prevention of fibrillation by antiarrhythmic drugs decreased the purine release in a highly significant way. After only 2 min of ischemia, reperfusion did not lead to ventricular fibrillation. Electrical induction of fibrillation during the reperfusion in these hearts provoked the release of very high amounts of the purine compounds. A similar effect of electrically-induced fibrillation was also obtained in hearts without a previous ischemic period. The findings suggest that ventricular fibrillation is able to induce the release of purine derivatives from the heart.
在离体灌注大鼠心脏中，造成了2分钟、5分钟和15分钟的全心缺血。根据缺血持续时间，缺血后再灌注导致腺苷及其代谢产物的释放，并引发或多或少严重的室性心律失常。当发生心室颤动时，与未发生颤动的心脏相比，嘌呤释放量显著增加。用抗心律失常药物预防颤动可显著降低嘌呤释放量。仅缺血2分钟后，再灌注未导致心室颤动。在这些心脏的再灌注过程中通过电刺激诱发颤动会引发大量嘌呤化合物的释放。在没有先前缺血期的心脏中，电刺激诱发颤动也获得了类似的效果。这些发现表明，心室颤动能够诱导心脏释放嘌呤衍生物。
