首页> 外文期刊>American Journal of Physiology >Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes.
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Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes.

机译:糖尿病大鼠神经源性介导的膀胱收缩反应的变化。

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Diabetic bladder dysfunction (DBD) is among the most common and bothersome complications of diabetes mellitus. Autonomic neuropathy has been counted as the cause of DBD. In the present study, we compared the alterations in the neurogenically mediated contractile responses of urinary bladder in rats with streptozocin-induced diabetes, 5% sucrose-induced diuresis, and age-matched controls. Male Sprague-Dawley rats were divided into three groups: 9-wk diabetic rats, diuretic rats, and age-matched controls. Micturition and morphometric characteristics were evaluated using metabolic cage and gross examination of the bladder. Bladder detrusor muscle strips were exposed to either periodic electrical field stimulation (EFS) or to EFS in the presence of atropine, alpha,beta-methylene adrenasine 5'-triphosphate, or tetrodotoxin. The proportions of cholinergic, purinergic, and residual nonadrenergic-noncholinergic (NANC) components of contractile response were compared among the three groups of animals. Diabetes caused a significant reduction of body weight compared with diuresis and controls, although the bladders of diabetic and diuretic rats weighed more than the controls. Both diabetes and diuresis caused significant increase in fluid intake, urine output, and bladder size. Diabetes and diuresis caused similarly increased response to EFS and reduced response to cholinergic component compared with controls. However, the purinergic response was significantly smaller in diuretic bladder strips compared with controls but not in diabetic rats. A residual NANC of unknown origin increased significantly but differently in diabetics and diuretics compared with controls. In conclusion, neurogenically mediated bladder contraction is altered in the diabetic rat. Diabetic-related changes do not parallel diuretic-induced changes, indicating that the pathogenesis of DBD needs further exploration.
机译:糖尿病性膀胱功能障碍(DBD)是糖尿病中最常见和最麻烦的并发症之一。自主神经病已被认为是引起DBD的原因。在本研究中,我们比较了链脲佐菌素诱导的糖尿病,5%蔗糖诱导的利尿和年龄匹配的对照组大鼠神经源性介导的膀胱收缩反应的变化。将雄性Sprague-Dawley大鼠分为三组:9周糖尿病大鼠,利尿大鼠和年龄匹配的对照组。使用代谢笼和大体检查膀胱来评估排尿和形态特征。将膀胱逼尿肌条暴露于周期性电场刺激(EFS)或在阿托品,α,β-亚甲基肾上腺素5'-三磷酸或河豚毒素的存在下暴露于EFS。在三组动物之间比较了胆碱能,嘌呤能和残余非肾上腺素能非胆碱能(NANC)收缩反应成分的比例。与利尿剂和对照组相比,糖尿病导致体重显着降低,尽管糖尿病和利尿大鼠的膀胱比对照组重。糖尿病和利尿均导致体液摄入,尿量和膀胱大小显着增加。与对照组相比,糖尿病和利尿引起的对EFS的反应相似,对胆碱能成分的响应降低。然而,与对照组相比,利尿膀胱条中的嘌呤能反应明显较小,而糖尿病大鼠则没有。与对照组相比,未知来源的残余NANC在糖尿病和利尿剂中显着增加,但有所不同。总之,在糖尿病大鼠中神经源性介导的膀胱收缩发生改变。糖尿病相关的变化与利尿剂引起的变化不平行,这表明DBD的发病机理需要进一步探讨。

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