Steen B Kristiansen, Ole Henning, Jens Erik Nielsen-Kudsk, Hans Erik Bøtker, Torsten Toftegaard Nielsen
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At each time point hearts were frozen in liquid nitrogen (-196 degrees C) within 2 seconds and myocardial contents of glycogen, lactate, alanine and glutamate were determined. Left ventricular pressure was measured continuously. Fasting and L-glutamate supplementation improved LV function after ischemia (Fast: p < 0.05, Glt: p < 0.01) and delayed myocardial glycogen depletion (Fast: p < 0.05, Glt: p < 0.01) compared to control. Decreased lactate accumulation and increased alanine content during ischemia were found in fasted (lactate: p < 0.05, alanine: p < 0.05) and L-glutamate supplemented (lactate: p < 0.01, alanine: p < 0.01) hearts compared to control. We did not find any additive effects of fasting and L-glutamate supplementation. In conclusion fasting and L-glutamate supplementation improve left ventricular function during reperfusion and delay myocardial glycogen depletion during ischemia. There were no additive effects of Fasting and L-glutamate supplementation. 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引用次数: 0
摘要
内源性糖原储存是维持心肌缺血时细胞功能所必需的。空腹和谷氨酸可改善缺血发作后左心室功能。我们研究了它们对缺血时心肌糖原消耗和再灌注时左心室功能和糖原再合成的影响。我们将185只Wistar大鼠分为4组:1)对照,2)禁食,16-20小时(Fast), 3)补充l -谷氨酸[100 mM] (Glt)或4)禁食+补充l -谷氨酸[100 mM]。每组N = 8-10。将心脏植入离体灌注大鼠心脏模型,稳定20分钟,缺血10/20/30分钟,再灌注60分钟。在每个时间点将心脏在-196℃液氮中冷冻2秒,测定心肌中糖原、乳酸、丙氨酸和谷氨酸的含量。连续测量左心室压。与对照组相比,禁食和补充l -谷氨酸可改善缺血后左室功能(Fast: p < 0.05, Glt: p < 0.01)和延迟心肌糖原消耗(Fast: p < 0.05, Glt: p < 0.01)。与对照组相比,空腹(乳酸:p < 0.05,丙氨酸:p < 0.05)和补充l -谷氨酸(乳酸:p < 0.01,丙氨酸:p < 0.01)心肌缺血时乳酸积累减少,丙氨酸含量增加。我们没有发现禁食和补充l -谷氨酸的任何附加效应。综上所述,空腹和补充l -谷氨酸可改善再灌注时左心室功能,延缓缺血时心肌糖原耗竭。禁食和补充l -谷氨酸没有附加效应。这些发现提示了l -谷氨酸补充和禁食的共同代谢途径。
Effects of L-glutamate supplementation mimic effects of fasting in the ischemic heart.
Endogenous glycogen stores are essential to maintain cell functions during myocardial ischemia.. Fasting and L-glutamate improve left ventricular function after an ischemic episode. We studied their effects on myocardial glycogen depletion during ischemia and on left ventricular function and glycogen resynthesis during reperfusion. We allocated 185 Wistar rats to 4 groups: 1) Control, 2) Fasting, 16-20 hours (Fast) 3) L-glutamate supplementation [100 mM] (Glt) or 4) Fasting + L-glutamate supplementation [100 mM]. n = 8-10 in each group. Hearts were mounted in an isolated perfused rat hearts model for 20 min stabilisation, 10/20/30 min ischemia and 60 min reperfusion. At each time point hearts were frozen in liquid nitrogen (-196 degrees C) within 2 seconds and myocardial contents of glycogen, lactate, alanine and glutamate were determined. Left ventricular pressure was measured continuously. Fasting and L-glutamate supplementation improved LV function after ischemia (Fast: p < 0.05, Glt: p < 0.01) and delayed myocardial glycogen depletion (Fast: p < 0.05, Glt: p < 0.01) compared to control. Decreased lactate accumulation and increased alanine content during ischemia were found in fasted (lactate: p < 0.05, alanine: p < 0.05) and L-glutamate supplemented (lactate: p < 0.01, alanine: p < 0.01) hearts compared to control. We did not find any additive effects of fasting and L-glutamate supplementation. In conclusion fasting and L-glutamate supplementation improve left ventricular function during reperfusion and delay myocardial glycogen depletion during ischemia. There were no additive effects of Fasting and L-glutamate supplementation. These finding suggest common metabolic pathways underlying the effects of L-glutamate supplementation and fasting.