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醛糖还原酶抑制剂索比尼尔不能预防糖尿病大鼠肛门尾骨肌中一氧化氮介导的神经传递损伤。

The aldose reductase inhibitor sorbinil does not prevent the impairment in nitric oxide-mediated neurotransmission in anococcygeus muscle from diabetic rats.

作者信息

Way K J, Reid J J

机构信息

Department of Medical Laboratory Science, Royal Melbourne Institute of Technology, Melbourne, Victoria, Australia.

出版信息

Eur J Pharmacol. 1996 Dec 27;318(1):101-8. doi: 10.1016/s0014-2999(96)00751-0.

Abstract

This study investigated whether increased polyol pathway activity could contribute to alterations in nitrergic neurotransmission in anococcygeus muscles from 8-week diabetic rats. In the presence of guanethidine (10-30 microM) and clonidine (0.01-0.05 microM), relaxations obtained to nitrergic nerve stimulation (0.5-5 Hz, 10-s train), to sodium nitroprusside (5-500 nM) and to nitric oxide (0.1-3 microM) were significantly reduced in muscles from diabetic rats compared to responses from control rats. Treatment of diabetic rats with the aldose reductase inhibitor sorbinil (42 mg/kg per day via feed for 8 weeks) did not affect impaired reactivity to nitrergic nerve stimulation, sodium nitroprusside or nitric oxide. The results suggest increased polyol pathway activity does not contribute to the alterations in nitrergic neurotransmission in anococcygeus muscles from diabetic rats.

摘要

本研究调查了多元醇途径活性增加是否会导致8周龄糖尿病大鼠的尾骨肌中一氧化氮能神经传递的改变。在胍乙啶(10 - 30微摩尔)和可乐定(0.01 - 0.05微摩尔)存在的情况下,与对照大鼠的反应相比,糖尿病大鼠肌肉中对一氧化氮能神经刺激(0.5 - 5赫兹,10秒串刺激)、硝普钠(5 - 500纳摩尔)和一氧化氮(0.1 - 3微摩尔)的松弛反应显著降低。用醛糖还原酶抑制剂索比尼尔(每天42毫克/千克,经饲料给药8周)治疗糖尿病大鼠,并不影响对一氧化氮能神经刺激、硝普钠或一氧化氮的反应受损情况。结果表明,多元醇途径活性增加不会导致糖尿病大鼠尾骨肌中一氧化氮能神经传递的改变。

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