Lagerstrom C F, Walker W E, Taegtmeyer H
Division of Thoracic and Cardiovascular Surgery, University of Texas Medical School, Houston.
Circ Res. 1988 Jul;63(1):81-6. doi: 10.1161/01.res.63.1.81.
We tested the hypothesis that depletion of glycogen prior to myocardial ischemia diminishes lactate buildup and improves functional recovery on reperfusion in the isolated rabbit heart. Cardiac glycogen was reduced either by substituting N2 for O2 in the perfusate or by perfusion with substrate-free solution, before the onset of ischemia. Hearts were subjected to either 30 minutes of normothermic (37 degrees C) or 60 minutes of hypothermic (4 degrees C) ischemia followed by 30 minutes of reperfusion with oxygenated Krebs-Henseleit buffer. Function was assessed by measuring peak left ventricular pressure at end-diastolic pressures ranging from 0 to 20 mm Hg. N2 perfusion for 15 minutes lowered myocardial glycogen by 60% and decreased ATP and phosphocreatine (p less than 0.001). Glycogen depletion did not decrease lactate accumulation during ischemia, but it impaired recovery with reperfusion (-46%, p less than 0.05). N2 perfusion for 5 minutes also reduced glycogen by 60%, but energy-rich phosphates were not reduced and functional recovery was still impaired (-40%, p less than 0.05). Perfusion with substrate-free medium diminished glycogen by 33% (p less than 0.05). Although lactate accumulation was significantly reduced (-45%, p less than 0.05), recovery following reperfusion was not improved. The results suggest that preservation of glycogen stores, but not the prevention of lactate buildup during ischemia, is beneficial for the recovery of function with reperfusion.
在心肌缺血前耗尽糖原可减少乳酸堆积，并改善离体兔心脏再灌注时的功能恢复。在缺血开始前，通过用N₂替代灌注液中的O₂或用无底物溶液灌注来减少心脏糖原。心脏分别经历30分钟的常温（37℃）或60分钟的低温（4℃）缺血，随后用含氧的克雷布斯 - 亨泽莱特缓冲液进行30分钟的再灌注。通过在舒张末期压力为0至20mmHg范围内测量左心室峰值压力来评估功能。用N₂灌注15分钟可使心肌糖原降低60%，并降低ATP和磷酸肌酸（p<0.001）。糖原耗尽在缺血期间并未减少乳酸积累，但损害了再灌注时的恢复（-46%，p<0.05）。用N₂灌注5分钟也可使糖原降低60%，但富含能量的磷酸盐未降低，功能恢复仍受损（-40%，p<0.05）。用无底物培养基灌注可使糖原减少33%（p<0.05）。虽然乳酸积累显著减少（-45%，p<0.05），但再灌注后的恢复并未改善。结果表明，保存糖原储备对再灌注时的功能恢复有益，而在缺血期间防止乳酸堆积并无益处。
