Perugia urodynamic method of analysis (PUMA): a new advanced method of urodynamic analysis applied clinically and compared with other advanced methods.

AIMS: The aim of this study is to compare PUMA curves with different pathologic conditions causing bladder dysfunction in 158 men and 83 women. METHODS: PUMA results in terms of bladder outlet obstruction and detrusor contractility were compared in 92 men with benign prostatic hypertrophy (BPH) and p(ves) congruent with p(det) (i.e., p(abd) congruent with 0) with the results of the urodynamics operator's opinion, the provisional International Continence Society method, Abrams and Griffith's diagram, urethral resistence factor (URA), Sch?fer's diagram, and Watt factor. PUMA curves correlated reliably with different pathologic conditions such as obstructive BPH, orthotopic bladder, cystocele, the neurological bladder, and bladder diverticulum. Statistical analysis indicated excellent agreement between PUMA and URA; agreement with other methods was good in cases of obstruction and nonobstruction. In doubtful cases, as diagnosed by standard methods, PUMA agreed only with the Abrams and Griffith's diagram. PUMA and Wmax were in good agreement on detrusor con traction force. Agreement between PUMA and Sch?fer's diagram was excellent for patients with detrusor hypercontractility and good for patients with detrusor hypocontractility and normocontractility. PUMA is the only method applicable to women. It is easy to perform. When integrated with other diagnostic tests, it provides realistic data for diagnosis, medical or surgical therapy, and outcome.     

手术治疗伴逼尿肌乏力的前列腺增生症

目的探讨BPH并有逼尿肌乏力(ACD)的病人是否手术等问题,为BPH并有逼尿肌乏力的病人治疗方法的选择提供依据.方法对尿动力学检查确认有ACD的15例BPH进行手术治疗.手术后复查尿流率.对所得数据进行自身配对t检验.结果术前和术后最大尿流率分别为(3.3±3.1)ml/s和(14.88±6.08)ml/s(P＜0.05).结论在前列腺摘除后,BPH伴有逼尿肌乏力的病人也能够产生有效排尿.故对确有膀胱出口梗阻(BOO)存在的BPH病人,即使有逼尿肌收缩乏力,也应积极手术.     

下尿路梗阻性肾积水患者逼尿肌功能变化

目的：探讨下尿路梗阻性肾积水患者逼尿肌功能变化。方法：对20例（3．5－73岁）下尿路梗阻导致的肾积水组和10例（13－67岁）无肾积水的对照组进行膀胱压力容积测定与压力－流率测定，并记录不同膀胱灌注量的逼尿肌基础压力。结果：下尿路梗阻性肾积水组逼尿肌－括约肌协同失调（DSD）11例（55％），逼尿肌功能过度活跃5例；而对照组仅发现1例（10％）DSD，未发现有逼尿肌功能过度活跃。下尿路梗阻性肾积水组平均膀胱顺应性显著低于对照组（P＜0．05），而下尿路梗阻性肾积水组平均逼尿肌基础压力，平均逼尿肌最大收缩压和残余尿量均显著高于对照组（P＜0．05），且下尿路梗阻性肾积水组在灌注量逐渐增加时高逼尿肌基础压力发生率逐渐增加。结论：下尿路梗阻性肾积水多伴有逼尿肌功能异常，提示膀胱逼尿肌功能改变与下尿路梗阻性肾积水的形成及发展有一定的相关性。     

Neuro-ophthalmic manifestations of the syndrome of ophthalmoplegia, ataxia and areflexia Observations on 20 patients

The neuro-ophthalmological manifestations of 20 patients with the syndrome of ophthalmoplegia, ataxia and areflexia are described. The symmetrical nature of the ophthalmoplegia and the associated cerebellar ataxia point to centrally placed lesions. Several supranuclear, nuclear and internuclear ophthalmological signs are identified. Some of these, like partial sparing of the levator palpebrae and normal downgaze in the presence of severe ophthalmoplegia are noted too frequently to be just unusual signs of peripheral oculomotor dysfunction. Other identified features included upper lid retraction on attempted upgaze and preserved Bell's phenomenon in the presence of paralysis of the latter, as well as several other central ophthalmological signs. These findings contrast with those seen in the Guillain-Barré syndrome and, thus, the syndrome of ophthalmoplegia, ataxia and areflexia is not a mere variant of it.     

老龄大鼠膀胱逼尿肌对神经递质反应的研究

目的 探讨老年排尿功能障碍的神经机制。方法 利用水浴条件下离体逼尿肌条张力测定技术，观察老龄Wistar大鼠膀胱逼尿肌条对不同浓度卡巴可、去甲肾上腺素、ATP的收缩反应改变；阿托品对卡巴可诱导逼尿肌收缩的舒张反应改变；异丙肾上腺素对电刺激诱导逼尿肌收缩的舒张反应改变。结果 与青龄组相比，老龄大鼠膀胱逼尿肌对ATP的收缩反应显著增强，对异丙肾上腺素的舒张反应在高浓度时增强；对卡巴可、阿托品、去甲肾上腺素的反应没有差异。结论 老龄大鼠排尿功能障碍可能与β-肾上腺素能、嘌呤能神经改变有关。     

Mechanics and Ca2+-sensitivity of human detrusor muscle bundles studied in vitro

Mechanical properties of isolated smooth muscle strips from human urinary bladder were investigated in vitro. Bladder tissue was obtained from tumour-free wall regions of bladders from male patients undergoing cystectomy for bladder carcinoma. In intact muscle strips, activated with high-K⁺ solution, half-maximal force occurred at about 0.9 mm extracellular [Ca²⁺]. The length-active force relation was determined and the muscle strips were fixed for light and electron microscopy at optimal length for active force (I_o). The maximal active force per unit smooth muscle cross-sectional area was 208±49 mN/mm², n= 6. Chemically skinned preparations were obtained by treatment with triton X-100. These preparations had a steep [Ca²⁺]-force relation in the micromolar range which was influenced by calmodulin. The skinned preparations could be maximally activated by irreversible thiophosphorylation of the regulatory light chains. The force-velocity relation was determined in the maximally activated skinned muscle at 22 °C at 0.5 1_o. When the muscle was shortened by 10%, force was reduced by 35% whereas the maximal shortening velocity was little affected.     

Role of the forebrain in bladder overactivity following cerebral infarction in the rat

This study was undertaken to investigate the contribution of the forebrain to bladder overactivity induced by cerebral infarction (CI). CI was induced by left middle cerebral artery (MCA) occlusion in female SD rat. Two and a half hours after CI or a sham operation (SO) decerebration was performed in some animals to eliminate forebrain influences on voiding function. Then bladder activity was monitored during continuous infusion cystometrograms in awake rats for 2.5 h. The effects of cumulative intravenous doses of MK-801 (0.1-1.4 mg/kg), an NMDA (N-methyl-D-aspartate) glutamatergic receptor antagonist, or sulpiride (0.1-41.1 mg/kg), D(2) selective dopaminergic receptor antagonists were studied over a 1.5-h period beginning 5 h after MCA occlusion. Bladder capacity was reduced by 57.5% after CI. In CI rats decerebration increased bladder capacity by 62.5% of predecerebration capacity. In SO rats bladder capacity was reduced by 25% after decerebration. MK-801 (0.4 and 1.4 mg/kg) increased bladder capacity in CI and CI-decerebrate rats, but did not change bladder capacity in SO-decerebrate rats. MK-801 decreased (60.7%) bladder capacity in SO-nondecerebrate rats. Sulpiride (11.1 and 41.1 mg/kg) significantly increased bladder capacity in CI, CI-decerebrate, and SO-decerebrate rats, but had no effect in SO-nondecerebrate rats. These results indicate that CI-induced decrease in bladder capacity is mediated by two mechanisms: (1) upregulation of an excitatory pathway from the forebrain, an effect blocked by decerebration and (2) downregulation of a tonic inhibitory pathway from the forebrain. The latter effect which can be induced by decerebration as well as CI unmasks a D(2) dopaminergic excitatory mechanism. An NMDA excitatory mechanism also contributes to the bladder overactivity after CI, but not after decerebration.