Przyklenk K
Department of Internal Medicine, Wayne State University and Harper Hospital, Detroit, MI.
Free Radic Biol Med. 1988;4(1):39-44. doi: 10.1016/0891-5849(88)90009-3.
A brief, transient period of coronary artery occlusion (less than 20 minutes in duration) followed by reperfusion does not result in irreversible myocyte injury or death, yet the regional contractile function and high energy phosphate content of the previously ischemic tissue remains depressed or 'stunned' for hours to days following reperfusion. It has been suggested that this prolonged postischemic dysfunction of viable, previously ischemic myocardium may be a consequence of oxygen-derived free radicals generated during occlusion or at the time of reperfusion. Recent evidence demonstrates that free radical scavenging agents such as superoxide dismutase (SOD) + catalase, N-2-mercaptopropionylglycine, and allopurinol, administered prior to coronary artery occlusion, significantly enhance recovery of regional contractile function of the stunned, previously ischemic tissue. This improved contractile function was not, however, accompanied by improvements in high energy phosphate metabolism: infusion of SOD + catalase did not preserve ATP stores in the previously ischemic tissue. These data support the hypothesis that oxygen-derived free radicals contribute, at least in part, to the phenomenon of the stunned myocardium. The source or mechanisms of free radical production in the setting of brief, transient ischemia, however, remains to be elucidated.
短暂的冠状动脉闭塞（持续时间少于20分钟）后再灌注不会导致不可逆的心肌细胞损伤或死亡，但在再灌注后的数小时至数天内，先前缺血组织的局部收缩功能和高能磷酸盐含量仍会降低或“顿抑”。有人提出，存活的、先前缺血的心肌在缺血后出现的这种长期功能障碍可能是闭塞期间或再灌注时产生的氧自由基所致。最近的证据表明，在冠状动脉闭塞前给予超氧化物歧化酶（SOD）+过氧化氢酶、N-2-巯基丙酰甘氨酸和别嘌呤醇等自由基清除剂，可显著增强顿抑的、先前缺血组织的局部收缩功能的恢复。然而，这种收缩功能的改善并未伴随着高能磷酸盐代谢的改善：输注SOD+过氧化氢酶并不能维持先前缺血组织中的ATP储备。这些数据支持了氧自由基至少部分导致心肌顿抑现象的假说。然而，短暂、一过性缺血情况下自由基产生的来源或机制仍有待阐明。
