Carrington A L, Ettlinger C B, Calcutt N A, Tomlinson D R
Department of Pharmacology, Queen Mary and Westfield College, University of London, UK.
Diabetologia. 1991 Jun;34(6):397-401. doi: 10.1007/BF00403177.
This study describes reduced motor nerve conduction velocity and increased resistance to hypoxia-induced conduction failure in sciatic nerves of rats after four weeks of streptozotocin-induced diabetes (both effects were significant at p less than 0.05). These changes occurred in the absence of any deficit in the steady-state ouabain-sensitive adenosine triphosphatase (ATPase) activity of sciatic nerve endoneurial homogenates. The addition of 10 nmol/l insulin to endoneurial homogenates from control animals resulted in a 34% increase in ouabain-sensitive ATPase activity and a 19% reduction in ouabain-insensitive ATPase activity (both p less than 0.01). This stimulation of ouabain-sensitive ATPase activity by insulin did not occur in homogenates from diabetic rats. Treating diabetic rats daily with the aldose reductase inhibitor, imirestat (1 mg/kg) improved nerve conduction velocity (p less than 0.05) but was without effect upon the resistance to hypoxic conduction blockade or the deficit in insulin-stimulated ouabain-sensitive ATPase activity. These data suggest that in streptozotocin-diabetic rats the functional disorders of reduced motor nerve conduction velocity and increased resistance to hypoxic conduction blockade do not share a common aetiology and that impaired nerve conduction is not related to reduced maximal potential ouabain-sensitive ATPase activity.
本研究描述了链脲佐菌素诱导糖尿病四周后大鼠坐骨神经运动神经传导速度降低以及对缺氧诱导的传导衰竭的耐受性增加（两种效应在p小于0.05时均具有统计学意义）。这些变化发生在坐骨神经内膜匀浆的稳态哇巴因敏感型三磷酸腺苷酶（ATP酶）活性无任何缺陷的情况下。向对照动物的内膜匀浆中添加10 nmol/l胰岛素会导致哇巴因敏感型ATP酶活性增加34%，哇巴因不敏感型ATP酶活性降低19%（两者p均小于0.01）。胰岛素对哇巴因敏感型ATP酶活性的这种刺激在糖尿病大鼠的匀浆中未出现。每天用醛糖还原酶抑制剂依米司他（1 mg/kg）治疗糖尿病大鼠可改善神经传导速度（p小于0.05），但对缺氧传导阻滞耐受性或胰岛素刺激的哇巴因敏感型ATP酶活性缺陷无影响。这些数据表明，在链脲佐菌素诱导的糖尿病大鼠中，运动神经传导速度降低和对缺氧传导阻滞耐受性增加的功能障碍没有共同的病因，并且神经传导受损与最大电位哇巴因敏感型ATP酶活性降低无关。
