Kilgour R D, Riggs C E
Department of Movement Science and Physical Education, Florida State University, Tallahassee 32306.
Diabetes Res. 1987 Oct;6(2):77-80.
The purpose of this investigation was to compare the biochemical responses of normal and streptozotocin (STZ) diabetic rat hearts to myocardial ischemia. As expected, left ventricular peak systolic pressure (LVPSP) declined with the onset of ischemia. The time required to reach 75% (LVPSP75) and 50% (LVPSP50) of baseline LVPSP100 was significantly (p less than 0.05) more rapid in diabetic and iodoacetate-treated hearts when compared to control animals. Diabetic rats experienced a significant (p less than 0.05) reduction in myocardial glycogen levels with ischemia. Despite enhanced glycogenolysis in diabetic rat hearts, cardiac lactate failed to accumulate in significant amounts. Overall, myocardial ATP and CP levels declined, but the reduction appears not to be associated with the fall in LVPSP. The results confirm that ventricular pressure development decreases rapidly following iodoacetate treatment. Similar declines in function were observed in the diabetic heart suggesting that glycolytic pathway inhibition and/or diminished glycolytic flux is responsible for the reduction in left ventricular pressure during myocardial ischemia.
本研究的目的是比较正常和链脲佐菌素（STZ）诱导的糖尿病大鼠心脏对心肌缺血的生化反应。正如预期的那样，随着缺血的开始，左心室收缩压峰值（LVPSP）下降。与对照动物相比，糖尿病和碘乙酸处理的心脏达到基线LVPSP100的75%（LVPSP75）和50%（LVPSP50）所需的时间显著更快（p小于0.05）。糖尿病大鼠心肌缺血时心肌糖原水平显著降低（p小于0.05）。尽管糖尿病大鼠心脏的糖原分解增强，但心脏乳酸并未大量积累。总体而言，心肌ATP和CP水平下降，但这种下降似乎与LVPSP的下降无关。结果证实，碘乙酸处理后心室压力的发展迅速降低。在糖尿病心脏中观察到类似的功能下降，这表明糖酵解途径的抑制和/或糖酵解通量的减少是心肌缺血期间左心室压力降低的原因。
