Hemmila M R, Zelenock G B, D'Alecy L G
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622.
J Vasc Surg. 1993 Apr;17(4):661-8. doi: 10.1067/mva.1993.39830.
The neurologic effect of induced hyperglycemia in the postischemic period was investigated with a rat aortic occlusion model.
Sprague-Dawley rats weighing 200 to 350 gm were anesthetized, intubated, and ventilated with 1% to 1.5% halothane. Temperature was continuously monitored and maintained at 37 degrees +/- 0.5 degrees C. The chest was opened, the thymus excised, and the aortic arch exposed. Snares were placed around the aorta distal to the left subclavian artery and the right and left subclavian arteries. The three vessels thus isolated were occluded for 8 minutes. With snare release and withdrawal, the rats received an intraperitoneal injection of 5% dextrose in water (2 gm/kg) or an equivalent volume of 0.9% saline solution. In a second group of rats the administration of glucose or saline solution was delayed until 30 minutes after snare release. Blood samples for blood glucose determination were obtained before operation, before occlusion, immediately after occlusion, and 15, 30, 45, 60, and 240 minutes after occlusion. A neurologic deficit score was assigned at 1, 4, 18, and 24 hours after occlusion to quantify hindlimb neurologic deficit based on 15-point scale (0 = normal, 15 = severe deficit). Sham-operated rats received the same operation and injection, but the snares were only manipulated and not made occlusive.
The rats that were administered glucose immediately after snare release showed a statistically significant exacerbation of lower extremity neurologic deficit at 24 hours after occlusion (p < or = 0.05, Mann-Whitney U test). The sham-operated rats were normal (0 score) at 24 hours. Significant elevation of blood glucose (321 +/- 33 mg/dl) was seen in the glucose-injected rats at 15 minutes and continued for up to 4 hours after occlusion (p = 0.040 and 0.014, respectively; Student's t test).
Postischemic hyperglycemia immediately after a standard spinal cord ischemic stress worsens neurologic outcome.
采用大鼠主动脉阻断模型研究缺血后诱导高血糖的神经学效应。
将体重200至350克的Sprague-Dawley大鼠麻醉、插管并用1%至1.5%的氟烷进行通气。持续监测体温并维持在37摄氏度±0.5摄氏度。打开胸腔，切除胸腺，暴露主动脉弓。在左锁骨下动脉远端的主动脉以及左右锁骨下动脉周围放置圈套器。将这三根血管阻断8分钟。松开并移除圈套器后，大鼠腹腔注射5%葡萄糖水溶液（2克/千克）或等量的0.9%盐溶液。在第二组大鼠中，葡萄糖或盐溶液的给药延迟至松开圈套器后30分钟。在手术前、阻断前、阻断后即刻以及阻断后15、30、45、60和240分钟采集血样测定血糖。在阻断后1、4、18和24小时评定神经功能缺损评分，基于15分制（0 = 正常，15 = 严重缺损）量化后肢神经功能缺损。假手术大鼠接受相同的手术和注射，但仅操作圈套器而不进行阻断。
松开圈套器后立即给予葡萄糖的大鼠在阻断后24小时下肢神经功能缺损有统计学意义的加重（p≤0.05，Mann-Whitney U检验）。假手术大鼠在24小时时正常（评分为0）。注射葡萄糖的大鼠在15分钟时血糖显著升高（321±33毫克/分升），并在阻断后持续长达4小时（分别为p = 0.040和0.014；Student's t检验）。
标准脊髓缺血应激后立即出现的缺血后高血糖会使神经学预后恶化。
