NERVE BLOOD-FLOW IN EARLY EXPERIMENTAL DIABETES IN RATS - RELATION TO CONDUCTION DEFICITS
NERVE BLOOD-FLOW IN EARLY EXPERIMENTAL DIABETES IN RATS - RELATION TO CONDUCTION DEFICITS
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DOI：
10.1152/ajpendo.1991.261.1.e1
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发表时间：
1991-07-01
影响因子：
--
通讯作者：
LOW, PA
中科院分区：
文献类型：
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作者：
CAMERON, NE;COTTER, MA;LOW, PA
慢性实验性糖尿病中神经血流量的减少与传导受损有关。 最近，有报道称，这之前有一段时间的功能性充血。 本研究探讨了糖尿病病程从1 wk到4 mo的链脲佐菌素治疗大鼠坐骨神经内膜血流和功能的早期变化。 通过微电极极谱法和氢清除率监测硫丁巴比妥（Inactin）麻醉动物的血流。 早在糖尿病诱导后1周，它就减少了41%。 没有早期功能性充血的证据，血流保持44%，直至4个月。 在另一项研究中，通过葡萄糖输注引起高血糖的正常大鼠也急性诱导了类似的血流量减少。 在糖尿病动物中，供应腓肠肌和胫骨前肌的坐骨神经分支的传导速度与血流量相关。 使用一组用乙啶治疗的2个月糖尿病大鼠进一步测试这种联系。 治疗引起功能性肾上腺素能交感神经切断术，血流量增加至正常范围内。 糖尿病患者传导速度降低26%，经治疗后恢复正常。 这些观察结果支持这一假设，即高血糖引起的血流量减少和由此产生的神经内膜缺氧是糖尿病神经病变发展早期神经传导缺陷的重要因素。
A reduction in nerve blood flow in chronic experimental diabetes has been linked to impaired conduction. Recently, there have been reports that this is preceded by a period of functional hyperemia. The present investigation explored early changes in sciatic nerve endoneurial blood flow and function in streptozocin-treated rats with durations of diabetes from 1 wk to 4 mo. Blood flow was monitored by microelectrode polarography and hydrogen clearance in thiobutabarbital (Inactin)-anesthetized animals. It was reduced by 41% as early as 1 wk after diabetes induction. There was no evidence of an early functional hyperemia, flow remaining 44% depressed up to 4 mo. In another investigation, similar reductions in blood flow were acutely induced in normal rats rendered hyperglycemic by glucose infusion. In diabetic animals, conduction velocity in sciatic branches supplying gastrocnemius and tibialis anterior muscles was correlated with blood flow. The link was further tested using a group of 2-mo diabetic rats treated with guanethidine. Treatment caused a functional adrenergic sympathetomy, and blood flow increased to within the normal range. Conduction velocity, depressed by 26% with diabetes, was normalized by treatment. These observations support the hypothesis that hyperglycemia-induced blood flow reductions and resultant endoneurial hypoxia are important factors underlying nerve conduction deficits early in the development of diabetic neuropathy.