Calcutt N A, Jorge M C, Yaksh T L, Chaplan S R
Department of Pathology, University of California San Diego, La Jolla 92093, USA.
Pain. 1996 Dec;68(2-3):293-9. doi: 10.1016/s0304-3959(96)03201-0.
Rats developed tactile allodynia within days of the onset of diabetes and which persisted for up to 8 weeks. Allodynia was prevented by insulin therapy that maintained normoglycemia while established allodynia was reversed by insulin therapy and normoglycemia of days but not hours duration. Tactile allodynia persisted in diabetic rats that received enough insulin to maintain normal body and foot weights but remained hyperglycemic, whereas this therapy was sufficient to correct other nerve disorders in diabetic rats, including deficits of sensory and motor nerve conduction velocity, nerve blood flow and hyperalgesia during the formalin test. Treating diabetic rats with the aldose reductase inhibitor ICI 222155 did not prevent tactile allodynia. Tactile allodynia was of similar magnitude in diabetic rats and nerve injured control rats and diabetes did not alter the magnitude or time course of nerve injury-induced allodynia. Systemic lidocaine treatment alleviated tactile allodynia in nerve injured control rats and both sham-operated and nerve injured diabetic rats. The streptozotocin-diabetic rat develops tactile allodynia that appears to be related to prolonged periods of insulin deficiency or hyperglycemia and which is amenable to treatment with lidocaine. The model may be of use in investigating the efficacy of other potential therapeutic agents for treating painful diabetic neuropathy.
大鼠在糖尿病发病数天内就出现了触觉异常性疼痛，且这种情况持续长达8周。胰岛素治疗可预防异常性疼痛，该治疗能维持血糖正常，而已经确立的异常性疼痛可通过胰岛素治疗及持续数天而非数小时的血糖正常得以逆转。触觉异常性疼痛在接受足够胰岛素以维持正常体重和足部重量但仍处于高血糖状态的糖尿病大鼠中持续存在，而这种治疗足以纠正糖尿病大鼠的其他神经紊乱，包括感觉和运动神经传导速度、神经血流的缺陷以及福尔马林试验期间的痛觉过敏。用醛糖还原酶抑制剂ICI 222155治疗糖尿病大鼠并不能预防触觉异常性疼痛。糖尿病大鼠和神经损伤对照大鼠的触觉异常性疼痛程度相似，糖尿病并未改变神经损伤诱导的异常性疼痛的程度或时间进程。全身应用利多卡因治疗可减轻神经损伤对照大鼠以及假手术和神经损伤糖尿病大鼠的触觉异常性疼痛。链脲佐菌素诱导的糖尿病大鼠会出现触觉异常性疼痛，这似乎与长时间的胰岛素缺乏或高血糖有关，并且可用利多卡因治疗。该模型可能有助于研究其他潜在治疗药物治疗糖尿病性疼痛性神经病变的疗效。
