Vergely C, Maupoil V, Benderitter M, Rochette L
Laboratoire de Physiopathologie et Pharmacologie Cardiovasculaires Expérimentales, Facultés de Médecine et Pharmacie, Dijon, France.
Free Radic Biol Med. 1998 Feb;24(3):470-9. doi: 10.1016/s0891-5849(97)00282-7.
Ascorbyl free radical (AFR), can be considered as an atoxic and endogenous indicator of oxidative stress. The purpose of our experiments was to investigate the influence of the severity and length of ischemia on the extent of AFR release during myocardial ischemia and reperfusion. For that purpose, isolated perfused rat hearts were submitted to a global ischemia, either total (residual flow 0%) or low flow (residual flow 5%), of 20 or 60 min length. Coronary effluents were collected at different times of experimentation and analyzed with Electron Spin Resonance (ESR) spectroscopy. AFR ESR doublet (g = 2.0054, aH = 0.188 MT) was not detected in coronary effluents collected during control perfusion periods. Nevertheless, during low-flow ischemia, a weak AFR release was noted. Moreover, a sudden and massive AFR liberation was observed at the time of reperfusion: this AFR release was weaker after low-flow ischemia than after total ischemia and was enhanced when the duration of ischemia increased from 20 min to 60 min. The large liberation of AFR noticed during global total ischemia was associated with a greater depression in myocardial contractile function and a lower recovery in coronary flow. In conclusion, our study demonstrates that AFR production at the time of reperfusion depends on the duration and strength of the ischemia, and is related to free radical injury. According to previously described ascorbate/AFR properties, we can conclude that AFR liberation in coronary effluents could represent a marker of oxidative stress during ischemia and/or reperfusion of hearts. This AFR release could be considered a sign of the severity of the ischemic episode, and could be related to the functional impairment during reperfusion.
抗坏血酸自由基（AFR）可被视为氧化应激的一种无毒内源性指标。我们实验的目的是研究缺血的严重程度和时长对心肌缺血及再灌注过程中AFR释放程度的影响。为此，将离体灌注的大鼠心脏进行20或60分钟的全心缺血，缺血类型为完全缺血（残余血流量0%）或低流量缺血（残余血流量5%）。在实验的不同时间收集冠状动脉流出液，并用电子自旋共振（ESR）光谱进行分析。在对照灌注期收集的冠状动脉流出液中未检测到AFR的ESR双峰（g = 2.0054，aH = 0.188 mT）。然而，在低流量缺血期间，观察到有微弱的AFR释放。此外，在再灌注时观察到AFR突然大量释放：低流量缺血后的这种AFR释放比完全缺血后弱，且当缺血时长从20分钟增加到60分钟时增强。在全心完全缺血期间观察到的大量AFR释放与心肌收缩功能的更大程度抑制及冠状动脉血流的更低恢复相关。总之，我们的研究表明，再灌注时AFR的产生取决于缺血的时长和强度，且与自由基损伤有关。根据先前描述的抗坏血酸/AFR特性，我们可以得出结论，冠状动脉流出液中AFR的释放可能代表心脏缺血和/或再灌注期间氧化应激的一个指标。这种AFR释放可被视为缺血发作严重程度的一个标志，且可能与再灌注期间的功能损害有关。
