链脲佐菌素诱导的糖尿病对大鼠逼尿肌非胆碱能运动传递的抑制作用及其被索比尼尔的预防作用
Inhibitory effect of streptozotocin-induced diabetes on non-cholinergic motor transmission in rat detrusor and its prevention by sorbinil.
作者信息
Luheshi G N, Zar M A
机构信息
Department of Pharmacological Sciences, Medical School, Newcastle Upon Tyne.
出版信息
Br J Pharmacol. 1990 Oct;101(2):411-7. doi: 10.1111/j.1476-5381.1990.tb12723.x.
Abstract
- Non-cholinergic motor transmission in the urinary bladder of streptozotocin (STZ)-diabetic rats was studied by recording contractile activity of strips of detrusor in vitro. 2. The neurogenic contractile responses to electrical field stimulation (EFS) of atropine-treated detrusor strips were decreased in 4, 8 and 12 week STZ-diabetic rats. The decrease was most marked in 12 week diabetic rats and least in 4 week ones. 3. Concentration-response curves showed no change in sensitivity of the detrusor to acetylcholine (ACh) in diabetic rats. The maximum tension generated by ACh was similar in diabetic and non-diabetic animals. 4. The contractile responses to EFS at frequencies greater than or equal to 1 Hz were not maintained during stimulation. The 'fade' was significantly greater in detrusor strips of diabetic rats. 5. The contractile response of detrusor to EFS was significantly greater in 12 week diabetic rats treated with the aldose reductase inhibitor sorbinil, than in untreated 12 week diabetic rats. The sensitivity to ACh was similar in the two groups. 6. It is concluded that the reduction of the neurogenic non-cholinergic responses of detrusor to EFS in STZ-diabetic rats is probably caused by a reduction in the release of the non-cholinergic motor transmitter. The results are discussed in relation to bladder dysfunction in human diabetes mellitus.
摘要
- 通过记录体外培养的逼尿肌条的收缩活性，研究了链脲佐菌素（STZ）诱导的糖尿病大鼠膀胱中的非胆碱能运动传递。2. 阿托品处理后的逼尿肌条对电场刺激（EFS）的神经源性收缩反应在4周、8周和12周的STZ糖尿病大鼠中降低。这种降低在12周的糖尿病大鼠中最为明显，在4周的大鼠中最不明显。3. 浓度-反应曲线显示糖尿病大鼠逼尿肌对乙酰胆碱（ACh）的敏感性没有变化。ACh产生的最大张力在糖尿病和非糖尿病动物中相似。4. 在频率大于或等于1Hz的EFS刺激期间，收缩反应不能持续。糖尿病大鼠逼尿肌条中的“衰减”明显更大。5. 用醛糖还原酶抑制剂索比尼尔治疗的12周糖尿病大鼠的逼尿肌对EFS的收缩反应明显大于未治疗的12周糖尿病大鼠。两组对ACh的敏感性相似。6. 得出结论，STZ糖尿病大鼠逼尿肌对EFS的神经源性非胆碱能反应降低可能是由于非胆碱能运动递质释放减少所致。结合人类糖尿病的膀胱功能障碍对结果进行了讨论。
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