Diabetic neuropathy includes damage to neurons, Schwann cells and blood vessels. Rodent models of diabetes do not adequately replicate all pathological features of diabetic neuropathy, particularly Schwann cell damage. We, therefore, tested the hypothesis that combining hypertension, a risk factor for neuropathy in diabetic patients, with insulin-deficient diabetes produces a more pertinent model of peripheral neuropathy. Behavioral, physiological and structural indices of neuropathy were measured for up to 6 months in spontaneously hypertensive and age-matched normotensive rats with or without concurrent streptozotocin-induced diabetes. Hypertensive rats developed nerve ischemia, thermal hyperalgesia, nerve conduction slowing and axonal atrophy. Thinly myelinated fibers with supernumerary Schwann cells indicative of cycles of demyelination and remyelination were also identified along with reduced nerve levels of myelin basic protein. Similar disorders were noted in streptozotocin-diabetic rats, except that thinly myelinated fibers were not observed and expression of myelin basic protein was normal. Superimposing diabetes on hypertension compounded disorders of nerve blood flow, conduction slowing and axonal atrophy and increased the incidence of thinly myelinated fibers. Rats with combined insulinopenia, hyperglycemia and hypertension provide a model for diabetic neuropathy that offers an opportunity to study mechanisms of Schwann cell pathology and suggests that hypertension may contribute to the etiology of diabetic neuropathy.

中文翻译：

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高血压引起的周围神经病变以及高血压和糖尿病对大鼠神经结构和功能的综合影响。

糖尿病性神经病包括对神经元、雪旺氏细胞和血管的损害。糖尿病啮齿动物模型不能充分复制糖尿病神经病变的所有病理特征，尤其是雪旺氏细胞损伤。因此，我们检验了以下假设：将高血压（糖尿病患者神经病变的危险因素）与胰岛素缺乏型糖尿病相结合可产生更相关的周围神经病变模型。在有或没有并发链脲佐菌素诱导的糖尿病的自发性高血压和年龄匹配的正常血压大鼠中测量神经病变的行为、生理和结构指数长达 6 个月。高血压大鼠出现神经缺血、热痛觉过敏、神经传导减慢和轴索萎缩。还鉴定了具有指示脱髓鞘和髓鞘再生周期的额外施万细胞的薄有髓纤维以及髓鞘碱性蛋白的神经水平降低。在链脲佐菌素-糖尿病大鼠中也观察到了类似的疾病，只是没有观察到薄的髓鞘纤维并且髓鞘碱性蛋白的表达正常。糖尿病叠加高血压会导致神经血流障碍、传导减慢和轴索萎缩，并增加稀有髓纤维的发生率。合并胰岛素减少、高血糖和高血压的大鼠为糖尿病神经病变提供了一个研究雪旺细胞病理机制的机会，并表明高血压可能导致糖尿病神经病变的病因。