Kitajima S
Department of Urology, School of Medicine, Akita University, Japan.
Nihon Hinyokika Gakkai Zasshi. 1996 Jan;87(1):18-26. doi: 10.5980/jpnjurol1989.87.18.
Diabetic lower urinary tract disfunction is well known, however, precise mechanism of the lower urinary tract disfunction remains to be solved. The present study is to clarify the lower urinary tract disfunction of diabetic rats by simultaneously measuring bladder and urethral pressures.
Female wistar rats were administered with streptozotocin (STZ 65 mg/kg, i.p.) to induce diabetes mellitus. Bladder and urethral pressures during rhythmic bladder contractions were compared under urethane anesthesia (1.0 g/kg, i.v.) between the control rats, diabetic rats, and diuretic rats.
The bladder contraction pressures of diabetic rats were decreased initially, but returned to the control values at 8 weeks. Atropine (2.5 mg/kg, i.a.) produced a marked reduction of bladder contraction pressure in the 8 weeks diabetic rats. The diabetic rats showed an increase of urethral pressure simultaneously with an increase of bladder pressure in the initial phase of rhythmic bladder contraction which is totally blocked by striated muscle relaxant. This phenomenon was not observed in the control or diuretic rats. Both group showed an initial decrease of urethral pressure followed by bladder contraction and rhythmic contractions of the urethra.
Our results suggest that bladder muscarinic receptors of the 8 weeks diabetic rats are more dominant than those of the other groups, and Mahoney's 4th reflex (urethrosphincteric guarding reflex) is facilitated but Mahoney's 6th reflex (detruthodetrusor facilitative reflex) is suppressed in the diabetic rats. We think that in the diabetic rats, sensory inputs by bladder distension were weak and could not induce Mahoney's 6th reflex until certain threshold values. Diabetic rats might develop changes in the mode of spinal neuronal transmission.
糖尿病性下尿路功能障碍广为人知，然而，下尿路功能障碍的确切机制仍有待解决。本研究旨在通过同时测量膀胱和尿道压力来阐明糖尿病大鼠的下尿路功能障碍。
给雌性Wistar大鼠腹腔注射链脲佐菌素（STZ 65mg/kg）以诱导糖尿病。在氨基甲酸乙酯麻醉（1.0g/kg，静脉注射）下，比较对照大鼠、糖尿病大鼠和利尿大鼠在膀胱有节律收缩时的膀胱和尿道压力。
糖尿病大鼠的膀胱收缩压最初降低，但在8周时恢复到对照值。阿托品（2.5mg/kg，腹腔注射）使8周龄糖尿病大鼠的膀胱收缩压显著降低。糖尿病大鼠在膀胱有节律收缩的初始阶段，尿道压力随着膀胱压力的升高而升高，这一现象可被横纹肌松弛剂完全阻断。在对照大鼠或利尿大鼠中未观察到这种现象。两组均显示尿道压力最初降低，随后是膀胱收缩和尿道的节律性收缩。
我们的结果表明，8周龄糖尿病大鼠的膀胱毒蕈碱受体比其他组更占优势，并且糖尿病大鼠中Mahoney第四反射（尿道括约肌保护反射）增强，但Mahoney第六反射（逼尿肌-逼尿肌促进反射）受到抑制。我们认为，在糖尿病大鼠中，膀胱扩张的感觉输入较弱，直到达到一定阈值才能诱导Mahoney第六反射。糖尿病大鼠可能会出现脊髓神经元传递模式的改变。
