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再灌注期间通过增强氨基酸底物逆转缺血性损伤。

Reversal of ischemic damage with amino acid substrate enhancement during reperfusion.

作者信息

Lazar H L, Buckberg G D, Manganaro A J, Becker H, Maloney J V

出版信息

Surgery. 1980 Nov;88(5):702-9.

PMID:7434210
Abstract

Twenty dogs underwent 15 minutes of normothermic ischemic arrest and 30 minutes of reperfusion while on cardiopulmonary bypass. In 10 control dogs, the reperfusate blood was not modified. In 10 other dogs, the aorta was reclamped and the heart reperfused for 5 minutes with blood containing L-glutamate (0.026M). We measured coronary blood flow (microspheres), left ventricular (LV) metabolism [O2 content, adenosine triphosphate (ATP)], LV compliance (intraventricular balloon), and LV performance (balloon and Starling curves) before and 30 minutes after ischemia. Fifteen minutes of ischemic arrest produced significant depression in contractility and oxidative metabolism. L-Glutamate infusion resulted in higher oxygen uptakes (9.7 versus 6.9 cc/100 gm/min) and allowed more complete recovery of ATP content (80% versus 67%). Glutamate-treated hearts had more complete recovery in the rate of contraction, +dP/dt, (96% versus 68%), and relaxation, --dP/dt (99% versus 72%), the best recovery of compliance (74% versus 88%), and complete (100%) recovery of stroke work index (1.55% versus 0.87% gm - m/kg). We conclude that the addition of L-glutamate to reperfusate blood reverses ischemic damage. We suspect that l-glutamate acts by replenishing Krebs' cycle intermediates lost during ischemia, thereby stimulating oxidative metabolism and enhancing ATP production.

摘要

20只狗在体外循环下经历了15分钟的常温缺血性停搏和30分钟的再灌注。10只对照犬的再灌注血液未作处理。另外10只犬,重新夹闭主动脉,并用含L - 谷氨酸(0.026M)的血液使心脏再灌注5分钟。我们在缺血前和缺血后30分钟测量了冠状动脉血流量(微球法)、左心室(LV)代谢[氧含量、三磷酸腺苷(ATP)]、左心室顺应性(心室内球囊)和左心室功能(球囊和斯塔林曲线)。15分钟的缺血性停搏导致收缩力和氧化代谢显著降低。输注L - 谷氨酸导致更高的氧摄取量(9.7对6.9毫升/100克/分钟),并使ATP含量更完全恢复(80%对67%)。用谷氨酸处理的心脏在收缩速率、+dP/dt(96%对68%)和舒张速率、--dP/dt(99%对72%)方面恢复更完全,顺应性恢复最佳(74%对88%),每搏功指数完全(100%)恢复(1.55%对0.87%克 - 米/千克)。我们得出结论,向再灌注血液中添加L - 谷氨酸可逆转缺血损伤。我们怀疑L - 谷氨酸的作用是补充缺血期间丢失的三羧酸循环中间产物,从而刺激氧化代谢并增强ATP生成。

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