Stanley W C, Hall J L, Smith K R, Cartee G D, Hacker T A, Wisneski J A
Biodynamics Laboratory, University of Wisconsin, Madison.
Metabolism. 1994 Jan;43(1):61-9. doi: 10.1016/0026-0495(94)90158-9.
We assessed the effects of 4 weeks of streptozocin-induced diabetes on regional myocardial glycolytic metabolism during ischemia in anesthetized open-chest domestic swine. Diabetic animals were hyperglycemic (12.0 +/- 2.1 v 6.6 +/- .5 mmol/L), and had lower fasting insulin levels (27 +/- 8 v 79 +/- 19 pmol/L). Myocardial glycolytic metabolism was studied with coronary flow controlled by an extracorporeal perfusion circuit. Left anterior descending coronary artery (LAD) flow was decreased by 50% for 45 minutes and left circumflex (CFX) flow was constant. Myocardial glucose uptake and extraction were measured with D-[6-3H]-2-deoxyglucose (DG) and myocardial blood flow was measured with microspheres. The rate of glucose conversion to lactate and lactate uptake and output were assessed with a continuous infusion of [6-14C]glucose and [U-13C]lactate into the coronary perfusion circuit. Both diabetic and nondiabetic animals had sharp decreases in subendocardial blood flow during ischemia (from 1.21 +/- .10 to 0.43 +/- .08 mL.g-1.min-1 in the nondiabetic group, and from 1.30 +/- .15 to 0.55 +/- .11 in the diabetic group). Diabetes had no significant effect on myocardial glucose uptake or glucose conversion to lactate under either well-perfused or ischemic conditions. Forty-five minutes of ischemia resulted in significant glycogen depletion in the subendocardium in both nondiabetic and diabetic animals, with no differences between the two groups. Glycolytic metabolism is not impaired in hyperglycemic diabetic swine after 1 month of the disease when compared with that in normoglycemic nondiabetic animals. The myocardial content of the insulin-regulatable glucose transporter (GLUT 4) was measured in left ventricular biopsies.(ABSTRACT TRUNCATED AT 250 WORDS)
我们评估了链脲佐菌素诱导的糖尿病持续4周对麻醉开胸家猪缺血期间局部心肌糖酵解代谢的影响。糖尿病动物血糖升高（12.0±2.1对6.6±0.5 mmol/L），空腹胰岛素水平较低（27±8对79±19 pmol/L）。通过体外灌注回路控制冠状动脉血流来研究心肌糖酵解代谢。左前降支冠状动脉（LAD）血流减少50%持续45分钟，左旋支（CFX）血流保持恒定。用D-[6-³H]-2-脱氧葡萄糖（DG）测量心肌葡萄糖摄取和提取，用微球测量心肌血流量。通过向冠状动脉灌注回路持续输注[6-¹⁴C]葡萄糖和[U-¹³C]乳酸来评估葡萄糖转化为乳酸的速率以及乳酸摄取和输出。缺血期间，糖尿病和非糖尿病动物的心内膜下血流均急剧下降（非糖尿病组从1.21±0.10降至0.43±0.08 mL·g⁻¹·min⁻¹，糖尿病组从1.30±0.15降至0.55±0.11）。在灌注良好或缺血条件下，糖尿病对心肌葡萄糖摄取或葡萄糖转化为乳酸均无显著影响。45分钟的缺血导致非糖尿病和糖尿病动物的心内膜下糖原显著耗竭，两组之间无差异。与血糖正常的非糖尿病动物相比，患病1个月的高血糖糖尿病猪的糖酵解代谢未受损。在左心室活检中测量了胰岛素可调节的葡萄糖转运蛋白（GLUT 4）的心肌含量。（摘要截断于250字）
