Failure of glycogen depletion to improve left ventricular function of the rabbit heart after hypothermic ischemic arrest.
Failure of glycogen depletion to improve left ventricular function of the rabbit heart after hypothermic ischemic arrest.
复制标题
低温缺血性骤停后糖原消耗无法改善兔心脏的左心室功能。
DOI：
10.1161/01.res.63.1.81
复制
发表时间：
1988
影响因子：
20.1
通讯作者：
Taegtmeyer,H
中科院分区：
文献类型：
--
作者：
Lagerstrom,CF;Walker,WE;Taegtmeyer,H
我们检验了心肌缺血前消耗糖原减少乳酸积累和改善离体兔心脏再灌注功能恢复的假设。在缺血发作之前，通过用N2代替灌注液中的O2或通过用无基质溶液灌注来减少心脏糖原。心脏接受30分钟常温（37摄氏度）或60分钟低温（4摄氏度）缺血，然后用含氧Krebs-Henseleit缓冲液再灌注30分钟。通过测量舒张末期压力范围为0至20 mm Hg时的左心室峰值压力来评估功能。N2灌注15分钟使心肌糖原降低60%，ATP和磷酸肌酸降低（p <0.001）。糖原消耗并没有减少缺血期间的乳酸积累，但它损害了再灌注的恢复（-46%，p <0.05）。N2灌注5分钟也使糖原减少60%，但富含能量的磷酸盐没有减少，功能恢复仍然受损（-40%，p <0.05）。用无底物培养基灌注使糖原减少33%（p <0.05）。尽管乳酸积累显著减少（-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，但不是防止乳酸积累在缺血期间，是有益的功能恢复与再灌注。
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.