Perry M O, Shires G T, Albert S A
J Vasc Surg. 1984 Jul;1(4):536-40.
Following distal arterial and venous cannulations in both hind limbs of 10 dogs, left leg arterial pressure was reduced to less than 50 torr (group I) and 50 to 75 torr (group II). Muscle membrane potential difference (PD) measurements, muscle biopsies, and arterial and venous blood samples were taken at baseline, after 3 hours of ischemia, and following 3 hours of reperfusion. Blood gas tensions and blood and muscle metabolites were measured. Muscle creatine phosphate levels fell during the ischemic period, but the adenosine triphosphate concentration remained normal. The PD fell in both groups during ischemia and declined further after reperfusion (p greater than 0.01). The deterioration in cell membrane function occurred in spite of intracellular energy repletion and persisted after reperfusion. The PD appears to be a more sensitive indicator of ischemia-induced cell dysfunction than levels of blood or intracellular metabolites. The cause of the progressive fall in the membrane potential is uncertain, but it may be due to cytotoxicity produced by oxygen free radicals.
在10只犬的双后肢进行远端动静脉插管后，将左腿动脉压降至低于50托（I组）和50至75托（II组）。在基线、缺血3小时后以及再灌注3小时后，进行肌肉膜电位差（PD）测量、肌肉活检以及采集动脉和静脉血样。测量血气张力以及血液和肌肉代谢产物。在缺血期间肌肉磷酸肌酸水平下降，但三磷酸腺苷浓度保持正常。两组在缺血期间PD均下降，再灌注后进一步下降（p大于0.01）。尽管细胞内能量充足，但细胞膜功能仍发生恶化，且再灌注后持续存在。与血液或细胞内代谢产物水平相比，PD似乎是缺血诱导细胞功能障碍更敏感的指标。膜电位逐渐下降的原因尚不确定，但可能是由于氧自由基产生的细胞毒性所致。
