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血管紧张素转换酶抑制剂赖诺普利可使链脲佐菌素诱导的糖尿病大鼠运动神经传导功能障碍迅速逆转。

Rapid reversal of a motor nerve conduction deficit in streptozotocin-diabetic rats by the angiotensin converting enzyme inhibitor lisinopril.

作者信息

Cameron N E, Cotter M A, Robertson S

机构信息

Department of Biomedical Sciences, University of Aberdeen, Marischal College, UK.

出版信息

Acta Diabetol. 1993;30(1):46-8. doi: 10.1007/BF00572874.

DOI:10.1007/BF00572874
PMID:8392403
Abstract

The effect of treatment of rats with the angiotensin converting enzyme inhibitor lisinopril after 5 weeks of untreated streptozotocin-diabetes was examined by daily monitoring of sciatic motor conduction velocity to tibialis anterior muscle. Diabetes produced a 31.5% decrease in conduction velocity (P < 0.001). Lisinopril treatment caused a progressive improvement which was significant after 3 days (P = 0.002), full normalization being achieved by 6 days (P < 0.0001). After 7 days of treatment there followed a 7-day washout period in which no lisinopril was given. During this time conduction velocity declined to untreated diabetic levels over 3 days. A subsequent treatment period resulted in complete normalization of conduction velocity within 2 days (P < 0.0001). Thus, the marked functional effects seen for vasodilator treatment with lisinopril suggest that angiotension converting enzyme inhibitors may have potential therapeutic value in the treatment of diabetic neuropathy.

摘要

在链脲佐菌素诱导的糖尿病大鼠未经治疗5周后,通过每日监测坐骨神经至胫前肌的运动传导速度,研究血管紧张素转换酶抑制剂赖诺普利对大鼠的治疗效果。糖尿病导致传导速度降低31.5%(P<0.001)。赖诺普利治疗引起传导速度逐渐改善,3天后具有显著性(P = 0.002),6天时完全恢复正常(P<0.0001)。治疗7天后,有一个7天的洗脱期,在此期间未给予赖诺普利。在此期间,传导速度在3天内降至未治疗糖尿病大鼠的水平。随后的治疗期导致传导速度在2天内完全恢复正常(P<0.0001)。因此,赖诺普利血管扩张治疗所观察到的显著功能效应表明,血管紧张素转换酶抑制剂在糖尿病神经病变的治疗中可能具有潜在的治疗价值。

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Angiotensin converting enzyme inhibition prevents development of muscle and nerve dysfunction and stimulates angiogenesis in streptozotocin-diabetic rats.血管紧张素转换酶抑制可预防链脲佐菌素诱导的糖尿病大鼠肌肉和神经功能障碍的发展,并刺激血管生成。
Diabetologia. 1992 Jan;35(1):12-8. doi: 10.1007/BF00400846.