Cameron N E, Cotter M A, Ferguson K, Robertson S, Radcliffe M A
School of Biomedical Sciences, University of Aberdeen, Scotland, United Kingdom.
Diabetes. 1991 Dec;40(12):1652-8. doi: 10.2337/diab.40.12.1652.
The effects of alpha-receptor blockade on nerve conduction, hypoxic resistance, ouabain-sensitive Na(+)-K(+)-ATPase, nerve polyols, and capillary density were examined in streptozocin-induced diabetic (STZ-D) rats. Nondiabetic and untreated diabetic control groups were used. Diabetes duration was 2 mo. There were two treated diabetic groups. A "prevention" group received 5 mg/kg prazosin for 2 mo from the induction of diabetes. A "reversal" group was untreated for the 1st mo and was given prazosin for the subsequent month. Conduction was measured in motor nerves supplying tibialis anterior and gastrocnemius muscles and sensory saphenous nerve. Diabetes resulted in 15-29% reductions in conduction velocity (P less than 0.01). In the prevention group, conduction deficits were minimal compared with untreated diabetes (P less than 0.01). In the reversal group, motor conduction was also substantially improved, although sensory conduction was not significantly affected. In vitro measurement of sciatic nerve hypoxic resistance revealed a 49% increase in the time taken for compound action potential amplitude to reach half its initial value with diabetes (P less than 0.01). This was largely prevented by prazosin treatment (P less than 0.01), although treatment had a lesser effect in the reversal group. Treatment had no effect on nerve polyol levels or Na(+)-K(+)-ATPase activity. Functional improvements with prazosin were probably based on increased vasa nervorum perfusion. There was a 20% elevation of endoneurial capillary density (P less than 0.01) in both prevention and reversal groups. We conclude that vascular factors play an important role in the etiology of experimental diabetic neuropathy, and functional changes may be corrected by chronic vasodilator treatment.
在链脲佐菌素诱导的糖尿病（STZ-D）大鼠中，研究了α受体阻断对神经传导、缺氧耐受性、哇巴因敏感的Na(+)-K(+)-ATP酶、神经多元醇和毛细血管密度的影响。使用了非糖尿病和未治疗的糖尿病对照组。糖尿病病程为2个月。有两个治疗的糖尿病组。一个“预防”组在糖尿病诱导后2个月内接受5mg/kg哌唑嗪治疗。一个“逆转”组在第1个月未接受治疗，在随后的1个月给予哌唑嗪治疗。在供应胫前肌和腓肠肌的运动神经以及感觉隐神经中测量传导。糖尿病导致传导速度降低15%-29%（P<0.01）。在预防组中，与未治疗的糖尿病相比，传导缺陷最小（P<0.01）。在逆转组中，运动传导也有显著改善，尽管感觉传导没有受到显著影响。坐骨神经缺氧耐受性的体外测量显示，糖尿病时复合动作电位幅度达到其初始值一半所需的时间增加了49%（P<0.01）。哌唑嗪治疗在很大程度上预防了这种情况（P<0.01），尽管治疗在逆转组中的效果较小。治疗对神经多元醇水平或Na(+)-K(+)-ATP酶活性没有影响。哌唑嗪的功能改善可能基于神经血管灌注增加。在预防组和逆转组中，神经内膜毛细血管密度均升高了20%（P<0.01）。我们得出结论，血管因素在实验性糖尿病神经病变的病因中起重要作用，慢性血管扩张剂治疗可能纠正功能改变。
