Steffen J M
Indiana University School of Medicine, Physiology Section, Bloomington, Indiana 47405.
Cryobiology. 1988 Apr;25(2):94-101. doi: 10.1016/0011-2240(88)90002-8.
The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 degrees C) was produced by exposure to helox (80% helium:20% oxygen) at 0 +/- 1 degree C. Hyperglycemia was noted during the induction process (169 +/- 8 in control vs 326 +/- 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming (Tre of 33 +/- 1 degrees C) was reduced (153 +/- 16 mg/dl) significantly (P less than 0.05). Serum insulin was depressed during hypothermic induction (from 48 +/- 4 in controls to 19 +/- 3 microU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.
大鼠在体温过低期间似乎无法利用葡萄糖。本研究的目的是检查诱导期、体温过低期和复温期的碳水化合物稳态。将正常体温的动物分组安乐死作为时间对照进行比较。通过在0±1℃暴露于氦氧混合气(80%氦:20%氧)来产生体温过低(15℃)。在诱导过程中观察到高血糖(对照组为169±8,体温过低大鼠为326±49mg/dl)。在体温过低的4小时内血清葡萄糖进一步升高,但复温后(目标温度为33±1℃)显著降低(153±16mg/dl)(P<0.05)。血清胰岛素在体温过低诱导期间降低(从对照组的48±4降至体温过低大鼠的19±3μU/ml),在苏醒过程中仅略有升高,仍显著低于正常体温的动物。在体温过低诱导期间,肝脏、骨骼肌和心脏的糖原初始浓度分别降低了34%、68%和75%。在体温过低的4小时内,肝糖原进一步减少,而骨骼肌和心脏的糖原储备显著增加。在复温期间,肝糖原显著减少,而骨骼肌和心脏的糖原储备得以维持。这些数据表明,体温过低大鼠的高血糖可由糖原分解和胰岛素分泌不足来解释。此外,本研究表明在持续体温过低期间骨骼肌和心肌糖原得到补充,而复温期间肌肉糖原得以保留。