Glucose Metabolism during Ischemia Due to Excessive Oxygen Demand or Altered Coronary Flow in the Isolated Arterially Perfused Rabbit Septum
Glucose Metabolism during Ischemia Due to Excessive Oxygen Demand or Altered Coronary Flow in the Isolated Arterially Perfused Rabbit Septum
复制标题
离体动脉灌注兔隔膜中因过度需氧或冠状动脉血流改变引起的缺血期间的葡萄糖代谢
作者：
R. Marshall;K. Shine;M. Phelps;N. Ricchiuti
分离的经动脉灌注的兔室间隔适于研究由需氧量增加或冠状动脉血流改变引起的缺血期间的葡萄糖代谢。在37°C条件下，以1.5 ml/min灌注并以72/min的速率刺激隔膜，这是一种低功准备，其中葡萄糖利用、乳酸生成、氧气消耗和发展的张力至少在90分钟内保持稳定。在以90/min的速度引入配对刺激并将流量增加到3.5 ml/min时，在以90/min的速度引入配对刺激并将流量维持在1.5 ml/min时产生的需求性缺血期间，以及在以72/min的恒定刺激速率降低流量产生的低流量缺血期间，对隔膜的代谢和功能反应进行了评估。在无氧增加工作时，葡萄糖利用率比对照组增加了115±26%（±SKM），耗氧量增加了100±11%，乳酸生成增加了13±9%，产生张力增加了45±8%。与对照组相比，组织糖原、乳酸和乳酸：丙酮酸比值没有变化。在需求性缺血时，葡萄糖利用增加了116±24%，而氧气消耗仅增加了29±7%，乳酸生成增加了106±16%，发展张力下降了20±4%。与对照组和无氧增加工作相比，在需求引起的缺血期间，组织糖原含量显著降低，组织乳酸和乳酸丙酮酸比值显著升高。这些结果与在无氧增加工作期间加速葡萄糖氧化和在需求引起的缺血期间加速无氧糖酵解一致。严重低流量缺血时，葡萄糖利用率下降44±8%，张力和耗氧量分别下降80±8%和74±2%。本研究结果提示，当缺氧引起缺血时，也观察到葡萄糖代谢依赖于代谢终产物的残留灌注冲洗。
The isolated arterially perfused interventricular rabbit septum was adapted for the study of glucose metabolism during ischemia produced by either increased oxygen demand or altered coronary flow. The septum perfused at 1.5 ml/min and stimulated at a rate of 72/min at 37 °C was shown to be a low work preparation in which glucose utilization, lactate production, oxygen consumption, and developed tension were stable for at least 90 minutes. The metabolic and functional responses of the septum were evaluated during nonnoxic increased work produced by introducing a paired stimulus at 90/min and increasing flow to 3.5 ml/min, during demand-induced ischemia produced by introducing a paired stimulus at 90/min and maintaining flow at 1.5 ml/min, and during low flow ischemia produced by decreasing flow and maintaining stimulus rate constant at 72/min. During nonnoxic increased work, glucose utilization increased by 115 ± 26% (±SKM) over control, while oxygen consumption increased by 100 ± 11%, lactate production by 13 ± 9%, and developed tension by 45 ± 8%. Tigsue glycogen, lactate, and lactate:pyruvate ratios were unchanged compared to control. During demand-induced ischemia, glucose utilization increased by 116 ± 24%, while oxygen consumption increased only by 29 ± 7%, lactate production rose by 106 ± 16%, and developed tension declined by 20 ± 4%. Tissue glycogen content was significantly decreased and tissue lactate and lactaterpyruvate ratios were significantly increased during demand-induced ischemia compared to both control and nonnoxic increased work. These results are consistent with accelerated glucose oxidation during nonnoxic increased work and accelerated anaerobic glycolysis during demand-induced ischemia. During severe low flow ischemia, glucose utilization declined by 44 ± 8% while developed tension and oxygen consumption decreased by 80 ± 8% and 74 ± 2%, respectively. The results of this study suggest that the dependence of glucose metabolism in ischemia on residual perfusion for washout of metabolic end products is also observed when ischemia is produced by excessive oxygen demand.