Pisarenko O I, Novikova E B, Serebriakova L I, Tskitishvili O V, Ivanov V E
Biull Eksp Biol Med. 1985 Sep;100(9):280-2.
The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.
在麻醉犬的心肌缺血和再灌注过程中,研究了静脉输注谷氨酸(3毫克/千克/分钟)的效果。通过前降支和回旋支冠状动脉灌注不足诱导左心室缺血。在冠状动脉血流量减少60%后2分钟,谷氨酸减轻了缺血性收缩抑制。左心室收缩压下降了9%,而对照组为22%;dP/dt下降了16%,而对照组为29%;左心室收缩压心率乘积下降了16%,而对照组为31%。谷氨酸再灌注改善了心脏功能的恢复,而心肌耗氧量没有增加。输注谷氨酸导致缺血心肌对谷氨酸的摄取增加了2倍。由于谷氨酰胺合成的激活,它导致心脏停止释放氨,增强了丙氨酸的形成并伴有丙酮酸的利用,且乳酸生成没有变化。文中讨论了谷氨酸保护作用的机制。