Paulson D J, Schmidt M J, Romens J, Shug A L
Basic Res Cardiol. 1984 Sep-Oct;79(5):551-61. doi: 10.1007/BF01910484.
The metabolic and physiologic differences between low-flow and zero-flow ischemia of varying duration were compared in the isolated perfused rat heart. Hearts subjected to 60 and 90 minutes of zero-flow ischemia recovered less cardiac work than hearts subjected to low-flow ischemia. Low-flow ischemia caused a build-up of both myocardial long-chain acyl coenzyme A and acyl carnitine esters, while zero-flow ischemia produced no change in long-chain acyl carnitine and only a transient increase in long-chain acyl coenzyme A. High energy phosphate depletion was greater in zero-flow ischemia. Perfusion with excess free fatty acids decreased the recovery of cardiac work after low-flow ischemia but had no effect after repeated episodes of zero-flow ischemia. L-Acetylcarnitine improved the recovery of cardiac work after low-flow ischemia in hearts perfused with 0.4 and 1.2 mM palmitate. With zero-flow ischemia, L-acetylcarnitine had no effect on the recovery of cardiac work in hearts perfused with 0.4 mM palmitate and a slight but statistically significant effect with 1.2 mM palmitate. Possible protective mechanisms of L-acetylcarnitine against ischemic damage are discussed.
在离体灌注大鼠心脏中，比较了不同持续时间的低流量缺血和零流量缺血之间的代谢及生理差异。经历60分钟和90分钟零流量缺血的心脏，其恢复的心脏功低于经历低流量缺血的心脏。低流量缺血导致心肌长链酰基辅酶A和酰基肉碱酯积聚，而零流量缺血时，长链酰基肉碱无变化，长链酰基辅酶A仅短暂增加。零流量缺血时高能磷酸耗竭更严重。用过量游离脂肪酸灌注会降低低流量缺血后心脏功的恢复，但在反复零流量缺血后无影响。在灌注0.4 mM和1.2 mM棕榈酸的心脏中，L-乙酰肉碱可改善低流量缺血后心脏功的恢复。对于零流量缺血，L-乙酰肉碱在灌注0.4 mM棕榈酸的心脏中对心脏功恢复无影响，而在灌注1.2 mM棕榈酸的心脏中有轻微但具有统计学意义的影响。文中讨论了L-乙酰肉碱对抗缺血损伤的可能保护机制。
