Wright J G, Fox D, Kerr J C, Valeri C R, Hobson R W
Department of Surgery, Boston University School of Medicine, Boston, Massachusetts 02118.
J Surg Res. 1988 Jun;44(6):754-63. doi: 10.1016/0022-4804(88)90111-4.
The mechanisms of ischemia-reperfusion (I-R) injury in skeletal muscle remain controversial. We investigated the effect of the rate of reperfusion blood flow on I-R injury in an isolated in vivo canine gracilis muscle model in six anesthetized dogs. In all animals, both gracilis muscles were subjected to 6 hr of ischemia followed by 1 hr of reperfusion. During reperfusion, one gracilis artery was partially occluded to limit the rate of reperfusion blood flow to its preischemic rate (limited reperfusion, LR), while the contralateral artery was allowed to perfuse freely at a normal rate (normal reperfusion, NR). Muscle injury was quantified by histochemical staining (triphenyltetrazolium chloride, TTC) with computerized planimetry of the infarct size, and by spectrophotometric determination of technetium-99m pyrophosphate uptake. Endothelial permeability was quantified by measurement of gracilis muscle weight gain and 125I-albumin radioactivity after intravenous injection. Results are presented as the means +/- SEM, and differences are considered to be statistically significant if P less than 0.05 by Student's t test for paired data. LR resulted in significantly less blood flow (9.7 +/- 1.7 cc/min/100 g) when compared to NR (55.7 +/- 11.6 cc/min/100 g). I-R injury was significantly reduced by LR as evidenced by a decrease in TTC infarct size from 41 +/- 7% to 11 +/- 5%, and a decrease in technetium-99m pyrophosphate uptake from 512 +/- 20 to 163 +/- 44 X 10(3) counts/min/g. LR also significantly decreased the postreperfusion edema formation as evidenced by a reduction in the muscle weight gain from 27 +/- 6 to 9 +/- 1 g, and a reduction in the 125I-albumin radioactivity from 45 +/- 14 to 32 +/- 8 counts/min/g. These data suggest that the hyperemic rate of reperfusion blood flow is a significant factor in the pathophysiology of postreperfusion edema and that clinical control of reperfusion injury in skeletal muscle may be achieved by limiting the rate of reperfusion blood flow.
骨骼肌缺血再灌注（I-R）损伤的机制仍存在争议。我们在6只麻醉犬的离体活体犬股薄肌模型中研究了再灌注血流速率对I-R损伤的影响。在所有动物中，双侧股薄肌均经历6小时缺血，随后再灌注1小时。在再灌注期间，一侧股薄肌动脉部分闭塞，将再灌注血流速率限制为缺血前速率（有限再灌注，LR），而对侧动脉以正常速率自由灌注（正常再灌注，NR）。通过组织化学染色（氯化三苯基四氮唑，TTC）并利用计算机图像分析测量梗死面积，以及通过分光光度法测定99m锝焦磷酸盐摄取量来量化肌肉损伤。通过测量股薄肌重量增加以及静脉注射后125I-白蛋白放射性来量化内皮通透性。结果以平均值±标准误表示，采用配对数据的Student t检验，若P小于0.05，则认为差异具有统计学意义。与NR（55.7±11.6 cc/min/100 g）相比，LR导致的血流显著减少（9.7±1.7 cc/min/100 g）。LR显著减轻了I-R损伤，TTC梗死面积从41±7%降至11±5%，99m锝焦磷酸盐摄取量从512±20降至163±44×10(3)计数/分钟/克，证明了这一点。LR还显著减少了再灌注后水肿形成，肌肉重量增加从27±6降至9±1克，125I-白蛋白放射性从45±14降至32±8计数/分钟/克，证明了这一点。这些数据表明，再灌注血流的充血速率是再灌注后水肿病理生理学中的一个重要因素，并且通过限制再灌注血流速率可能实现骨骼肌再灌注损伤的临床控制。
