Postischemic hypothermia diminishes skeletal muscle reperfusion edema

Abstract

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°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. Reperfusion conditions Cold (CR) Warm (WR) P value Ischemic temperature (°C) 34 ± 1 34 ± 1 0.68 Reperfusion temperature (°C) 21 ± 3 34 ± 2 <0.05 pH just before hypothermia 5.97 ± 0.08 5.97 ± 0.06 0.89 pH just before reperfusion 6.40 ± 0.13 5.96 ± 0.05 <0.02 pH after 1 hr of reperfusion 6.77 ± 0.27 6.43 ± 0.29 <0.05 Muscle weight gain (g) 25 ± 4 46 ± 9 <0.05 125I-Alb (counts/min/g) 41 ± 8 45 ± 14 0.13 Postischemic hypothermia significantly increased the interstitial muscle pH and significantly reduced postre-perfusion 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.