Wright J G, Araki C T, Belkin M, Hobson R W
Division of Vascular Surgery, Ohio State University Medical Center, Columbus 43210.
J Surg Res. 1989 Nov;47(5):389-96. doi: 10.1016/0022-4804(89)90089-9.
The mechanisms of ischemia-reperfusion injury in skeletal muscle remain controversial. We investigated the ability of postischemic hypothermia to diminish reperfusion edema and improve skeletal muscle pH in a bilateral, in vivo isolated canine gracilis muscle model. In five anesthetized animals, both gracilis muscles were subjected to 6 hr of ischemia followed by 1 hr of reperfusion. After 5 hr of warm ischemia, one gracilis muscle was cooled to 21 degrees C (cold reperfusion, CR) while the contralateral gracilis muscle was maintained at ambient temperature (warm reperfusion, WR). Reperfusion muscle edema was quantitated by measurement of gracilis muscle weight gain. Interstitial muscle pH was monitored by glass microelectrodes. Vascular permeability was measured by analysis of albumin (125I-Alb) leak. Results are presented as the means +/- SEM. (table; see text) Postischemic hypothermia significantly increased the interstitial muscle pH and significantly reduced postreperfusion muscle edema, without changing the vascular permeability to albumin. These data suggest that hypothermia may provide a clinical method for salvaging ischemic skeletal muscle from the postreperfusion edema that can lead to compartment syndromes, reperfusion injury, and subsequent limb loss.
骨骼肌缺血再灌注损伤的机制仍存在争议。我们在双侧体内分离犬股薄肌模型中，研究了缺血后低温减轻再灌注水肿并改善骨骼肌pH值的能力。在五只麻醉动物中，双侧股薄肌均经历6小时缺血，随后1小时再灌注。在5小时热缺血后，一侧股薄肌冷却至21摄氏度（冷再灌注，CR），而对侧股薄肌维持在环境温度（热再灌注，WR）。通过测量股薄肌重量增加来定量再灌注肌肉水肿。用玻璃微电极监测肌间质pH值。通过分析白蛋白（125I-Alb）渗漏来测量血管通透性。结果以平均值±标准误表示。（表格；见正文）缺血后低温显著提高了肌间质pH值，并显著减轻了再灌注后肌肉水肿，而不改变血管对白蛋白的通透性。这些数据表明，低温可能提供一种临床方法，以挽救缺血骨骼肌免受可导致骨筋膜室综合征、再灌注损伤及随后肢体丧失的再灌注水肿。
