Malmgren A, Uvelius B, Andersson K E, Andersson P O
Department of Clinical Pharmacology, University of Lund, Sweden.
J Urol. 1992 Sep;148(3):930-4. doi: 10.1016/s0022-5347(17)36780-0.
Bladder function was investigated in female rats with hereditary diabetes insipidus (DI) and in healthy controls, in vivo by means of recordings of micturition pattern and cystometry, and in vitro in organ bath experiments. Rats with DI exhibited bladder hypertrophy, the weight of the bladder in these rats being two times that of controls. Recordings of micturition pattern showed that DI-rats had an increased 24 hour diuresis and micturition volume, and decreased micturition interval in comparison with controls. Cystometry recordings revealed increased bladder capacity and micturition volume in DI-rats. However, in these rats basal bladder pressure and threshold pressure were lower than in controls. No significant changes in micturition pressure or bladder compliance were observed, and none of the rats had residual urine. In organ bath studies, a lower maximal response to electrical field stimulation was obtained in bladder strips from DI-rats, than in the control strips, when expressed relative to the response elicited by K(+)-solution. When activated by field stimulation, the DI-bladder strips and the control strips had similar sensitivity to muscarinic receptor blockade with scopolamine at all stimulation frequencies. The sensitivity to carbachol was similar in the two groups. The results suggest that the increased functional demands of DI on the detrusor do not result in major changes pre- or postjunctionally. Further, several of the previously reported urinary bladder changes observed in rats with diabetes mellitus (DM) are similar to those now reported in rats with DI, emphasizing the importance of an increased diuresis per se for the development of alterations in bladder function. However, in contrast to the findings in DM rats, the sensitivity to electrical stimulation of nerves during blockade of muscarinic receptors was similar in DI-rats and their controls. This supports our previous suggestion that the increased resistance to muscarinic receptor blockade of the bladder in DM-rats at low stimulation frequencies is induced by the disease (diabetes mellitus) as such and not by the increased diuresis.
通过记录排尿模式和膀胱内压测量法在体内研究遗传性尿崩症(DI)雌性大鼠和健康对照大鼠的膀胱功能,并在离体器官浴实验中进行研究。DI大鼠出现膀胱肥大,这些大鼠的膀胱重量是对照大鼠的两倍。排尿模式记录显示,与对照相比,DI大鼠24小时尿量和排尿量增加,排尿间隔缩短。膀胱内压测量记录显示DI大鼠膀胱容量和排尿量增加。然而,这些大鼠的基础膀胱压力和阈值压力低于对照。未观察到排尿压力或膀胱顺应性有显著变化,且所有大鼠均无残余尿。在器官浴研究中,相对于K(+)溶液引发的反应,DI大鼠膀胱条对电场刺激的最大反应低于对照条。当通过电场刺激激活时,在所有刺激频率下,DI膀胱条和对照条对东莨菪碱的毒蕈碱受体阻断具有相似的敏感性。两组对卡巴胆碱的敏感性相似。结果表明DI对逼尿肌功能需求的增加不会导致神经节前或节后的重大变化。此外,先前报道的糖尿病(DM)大鼠膀胱变化中的一些与现在报道的DI大鼠相似,强调了尿量增加本身对膀胱功能改变发展的重要性。然而,与DM大鼠的发现相反,DI大鼠及其对照在毒蕈碱受体阻断期间对神经电刺激的敏感性相似。这支持了我们先前的观点,即DM大鼠在低刺激频率下膀胱对毒蕈碱受体阻断的抵抗力增加是由疾病(糖尿病)本身引起的,而非由尿量增加引起。