Hacker T A, Hall J L, Stone C K, Stanley W C
Biodynamics Laboratory, University of Wisconsin, Madison.
Basic Res Cardiol. 1992 Mar-Apr;87(2):184-92. doi: 10.1007/BF00801965.
Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9 +/- 0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27 +/- 0.16 to 0.25 +/- 0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p less than 0.05) and a switch to net lactate production (p less than 0.01). Ischemia did not affect the rates of alanine output (-0.9 +/- 1.0 vs. -0.3 +/- 0.3 mumol/min) or glutamate uptake (-0.4 +/- 1.1 vs. 0.3 +/- 0.6 mumol/min), but did increase the venous-arterial difference for ammonia (-4.1 +/- 4.1 to 52.7 +/- 5.5 microM, p less than 0.0001) and the ammonia output (-0.33 +/- 0.24 to 1.34 +/- 0.14 mumol/min, p less than 0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.
冠状动脉疾病会导致心脏对谷氨酸的摄取增加以及丙氨酸的输出增加。我们评估了急性心肌缺血对10头麻醉开胸家猪（体重46.9±0.7千克）丙氨酸和谷氨酸交换以及氨生成的影响。通过体外灌注回路控制冠状动脉血流。在非缺血对照期（有氧）后，左前降支冠状动脉血流减少60%。在缺血35分钟之前和期间采集动脉和前室间静脉样本。使用放射性微球测量的内膜下血流从1.27±0.16降至0.25±0.09（毫升/克）/分钟，左心室壁增厚降至有氧值的47%。缺血导致葡萄糖摄取率显著增加（p<0.05）并转变为净乳酸生成（p<0.01）。缺血不影响丙氨酸输出率（-0.9±1.0对-0.3±0.3微摩尔/分钟）或谷氨酸摄取率（-0.4±1.1对0.3±0.6微摩尔/分钟），但确实增加了氨的动静脉差值（-4.1±4.1至52.7±5.5微摩尔，p<0.0001）和氨输出（-0.33±0.24至1.34±0.14微摩尔/分钟，p<0.0001）。总之，急性缺血并未刺激更高的丙氨酸输出或谷氨酸摄取。然而，急性缺血确实导致无氧糖酵解速率和氨输出增加，这反映了心肌能量代谢的严重紊乱。
