逼尿肌活动过度伴收缩功能受损对膀胱排空的影响

目的探讨逼尿肌活动过度伴收缩功能受损(DHIC)对膀胱排空功能的影响。方法通过压力流率测定分别对99例DHIC和176例单纯逼尿肌收缩力减弱的患者(对照组)进行评估,对相应资料进行统计学分析。结果DHIC组患者的剩余尿量、最大尿流率(Qmax)、最大尿流率时逼尿肌压(PdetQmax)、膀胱顺应性、膀胱容量(V)分别为(106.40±149.55)ml、(5.91±3.24)ml/s、(44.52±17.78)cmH2O、(26.34±48.16)ml/cmH2O和(228.28±93.36)ml,对照组分别为(228.88±241.71)ml、(4.13±3.10)ml/s、(34.42±20.82)cmH2O、(66.96±97.53)ml/cmH2O和(328.30±123.19)ml,2组比较差异均有统计学意义(P<0.05)。有膀胱出口梗阻的DHIC(44例)与有梗阻的单纯逼尿肌收缩力减弱患者(52例)相比,剩余尿量、膀胱顺应性和V的差异有统计学意义(P<0.05)。口服黄酮哌酯或舍尼亭出现尿潴留者16例。有上尿路扩张者11例,其中DHIC者8例。结论DHIC的膀胱排空能力高于单纯逼尿肌收缩力减弱者。应谨慎应用抑制逼尿肌收缩的药物。DHIC患者膀胱顺应性较低,应警惕可能发生上尿路损害。     

Effects of pinacidil and cromakalim (BRL 34915) on bladder function in rats with detrusor instability

Normal rats as well as rats with bladder hypertrophy secondary to outflow obstruction were investigated cystometrically before and after administration of the potassium channel openers pinacidil or cromakalim one mg./kg. orally. In normal rats cromakalim decreased micturition pressure by 15 +/- 6%. A diminished micturition pressure was also seen after pinacidil (by 18 +/- 8%) but this did not achieve statistical significance. Further, no clear-cut effects on bladder capacity, residual volume, basal bladder pressure, threshold pressure, bladder compliance or on bladder wall tension were seen in this group of rats neither in the presence of pinacidil nor cromakalim. Rats with bladder hypertrophy exhibited a significant bladder instability during cystometrical investigations. The mean amplitude of the spontaneous bladder contraction exceeded 20 cm. H2O prior to micturition. Administration of pinacidil and cromakalin decreased the spontaneous contractions to 26 +/- 12% and 22 +/- 7%, respectively, of that seen in the absence of the drugs. Furthermore, pinacidil decreased micturition pressure by 61 +/- 12%. Also cromakalim decreased micturition pressure (by 27 +/- 13%) but this effect did not achieve statistical significance. After both pinacidil and cromakalim these rats tended to develop residual urine. In accordance with the results in normal rats pinacidil and cromakalim showed no effects on bladder capacity, basal bladder pressure, threshold pressure, bladder compliance or on bladder wall tension in rats with bladder hypertrophy. The findings of an almost complete disappearance of spontaneous bladder contractions in rats with bladder instability and a remaining voiding ability after administration of pinacidil or cromakalim suggest that potassium channel openers may be a therapeutic alternative in the treatment of bladder instability associated with outflow obstruction.     

前列腺增生症的逼尿肌功能观察

对８５例前列腺增生病人的逼尿肌功能进行了尿动力学观察，将前列腺梗阻性膀胱分为正常、反射亢进、低顺应和高顺应４种类型，并对其梗阻解除前后的逼尿肌功能变化进行了观察。尿动力学检查可判断逼尿肌功能状态及其损害程度，能准确掌握手术时机，强调在逼尿期尚未发生功能障碍之前，及时解除梗阻，最大限度地减少膀胱逼尿肌的去神经性损害。     

Residual urine,underactive detrusor function,and the nature of detrusor/sphincter dyssynergia

In a group of 280 patients with mixed pathology the adequacy of the detrusor contraction during voiding has been assessed by a new method. For the group as a whole, residual urine is nearly always the result of the fading away of the detrusor contraction and rarely of premature sphincter contraction. It is strongly associated with failure to attain an adequate detrusor contraction at any time during the micturition. The same is true both for children who show consistent urethral overactivity during voiding and for patients with detrusor/sphincter dyssynergia of neuropathic origin. The results suggest that in detrusor/sphincter dyssynergia or other types of urethral overactivity, it may be misleading to ascribe inefficient bladder emptying solely to the obstructive effect of the urethral closure mechanism; the underactive detrusor function should also be taken into account. Often there appears to be an incomplete activation of the micturition reflex, resulting in both incomplete stimulation of the detrusor and incomplete relaxation of the urethral closure mechanism.     

Effects of ligation of the internal iliac artery on blood flow to the bladder and detrusor function in rat

Ischaemia induced by atherosclerosis is a common cause of disorders in the elderly, including impairment of bladder function. To evaluate experimentally the effects of ischaemia on detrusor function, we performed infusion cystometry and evaluated the morphologic findings in the bladder of the rat. Blood flow to the bladder of the rat was evaluated with a Doppler flowmeter before and after the unilateral or bilateral ligation of the internal iliac arteries. Reevaluation was done at one and two weeks after surgery. Bladder function was studied by infusion cystometry performedin vivo under urethane anaesthesia. Finally, histological examination was performed. Blood flow at mid-dorsal wall of the control bladder was inversely related to intravesical volume. Unilateral or bilateral ligation of the internal iliac arteries decreased blood flow to the bladder, which showed a complete recovery two weeks postoperatively. Infusion cystometry of the ischaemic bladder with bilateral ligation of the internal iliac arteries demonstrated a decrease in voiding pressure, an increase in bladder capacity, and an increase in pressure at which micturition was initiated vs. the control. The bladder with unilateral ligation of the artery showed a decrease in voiding pressure, with no change in the other parameters. Histological examination indicated that the bilateral ischaemia and ischaemic side of unilateral ischaemia led to a degeneration of the mucosa, and severe oedema in submucosal and muscle layers one week postoperatively. Degeneration of smooth muscle was predominant at 2 weeks. Contralateral side of the unilaterally ischaemic bladder showed oedema and congestion of the submucosa and smooth muscle. Ligation of the internal iliac artery decreased blood flow to the bladder significantly, which resulted in smooth muscle degeneration. Consequently,in vivo voiding pressure was impaired in the ischaemic bladder.     

膀胱出口部分梗阻对逼尿肌生物力学特性的影响

目的 探讨膀胱出口部分梗阻(P-BOO)对膀胱逼尿肌生物力学特性的影响及机制.方法 采用Wistar雄性大鼠,膀胱颈不全结扎法建立P-BOO动物模型.依据梗阻时间分为假手术组、梗阻6周组(P-B006W)及梗阻12周组(P-B0012W),其中P-B006W组根据充盈性膀胱测压所示逼尿肌是否稳定分为逼尿肌稳定组(DS)和逼尿肌不稳定组(DI).采用灌流肌槽,以拟胆碱药物(氯化氨基甲酰胆碱)作为刺激因素,用拉力传感器测定离体逼尿肌条的主动收缩功能.充盈性膀胱测压检测最大膀胱容量、膀胱漏尿点压及膀胱顺应性的变化.结果P-BOO模型均成功建立,DI组最大膀胱容量、膀胱漏尿点压、膀胱顺应性[(10.8±3.0)ml,(39.4±7.1)cm H20,(0.27±0.08)ml/cm H20]、DS组[(10.3±1.9)ml,(35.9±6.2)cm H2O,(0.29±0.05)ml/cm H2O]及P-B0012W组[(9.5±2.3)ml,(48.6±9.5)cm H20,(0.21±0.05)ml/cm H2O]均明显高于假手术组[(2.1±0.3)ml,(16.2±2.1)cm H2O,(0.13±0.03)ml/cm H2O],差异有统计学意义(P＜0.05).DI组逼尿肌条拟胆碱药物刺激产生的收缩力显著低于假手术组和DS组.P-B0012W组逼尿肌条均未检测到明确的收缩波(波幅＜0.05 g).结论 P-BOO后膀胱逼尿肌生物力学特性发生了改变:DI组逼尿肌收缩功能受损,DS组发生代偿,但如果梗阻未解除,则逼尿肌收缩性损害,最终导致不可逆的收缩功能丧失;梗阻后膀胱顺应性增大与膀胱容积显著增加密切相关,逼尿肌稳定性对其影响不显著.     

良性前列腺增生患者逼尿肌功能的评估和治疗对策

目的　为了解良性前列腺增生（BPH）患者产生下尿路症状的成因,为正确诊治下尿路症状提供准确的证据。　方法　采用尿动力学方法分析无神经系统疾病的良性前列腺增生患者的膀胱尿道功能。　结果　164例良性前列腺增生患者,平均年龄67±7.04岁,膀胱出口梗阻者占61.6％（101/164）,无梗阻者占38.4％（63/164）;逼尿肌收缩力正常者为83%（136/164）,逼尿肌收缩力减弱者17％（28/164）,以上各组之间I-PSS评分和年龄无显著性差异。膀胱出口无梗阻者中逼尿肌收缩力减弱者占44.4%（28/63）,逼尿肌收缩力正常占55.6％（35/63）。在膀胱出口无梗阻者中,逼尿肌收缩力减弱合并不稳定膀胱患者为28.6％（8/28）,而逼尿肌收缩力正常合并不稳定膀胱患者57.1％（20/35）,膀胱出口无梗阻逼尿肌收缩力减弱合并不稳定膀胱患者明显少于膀胱出口无梗阻逼尿肌收缩力正常者（P＜0.02）,两组患者I-PSS评分和膀胱顺应性均无明显差异。　结论　BPH患者下尿路症状的产生不仅与前列腺增生引起的膀胱出口梗阻有关,部分患者并不存在膀胱出口梗阻,其下尿路症状的成因为逼尿肌功能变化所致,尿动力学检查能为下尿路症状患者的诊治提供可靠的依据。     

The actions of extracellular magnesium on isolated human detrusor muscle function.

The effects of increasing the extracellular magnesium concentration ([Mg]) on the in vitro mechanical and electrophysiological properties of isolated human detrusor smooth muscle have been investigated. Raising extracellular Mg reduced the magnitude of the electrically-induced phasic contractions as well as spontaneous contractions. A similar increase in the [Mg] reduced the magnitude of the inward Ca2+ current associated with the action potential as well as shifting the activation curve to more positive potentials. Spontaneous oscillations of intracellular Ca2+ could be observed in some isolated cells and such activity was also abolished by raising the extracellular [Mg]. It is proposed that the contractile effects of raised extracellular Mg are mediated by an action on the inward Ca2+ current and that these observations suggest a means whereby normal and abnormal detrusor contractions might be effectively regulated.     

Effects of chronic cadmium exposure on contractility of the rat detrusor

. The chronic effects of Cd²⁺ on the myogenic contractions induced by acetylcholine (ACh), and the neurogenic contractions induced by electrical field stimulation (EFS) of the rat detrusor were investigated. Wistar Kyoto rats weighing 150–250 g were randomly divided into four groups each containing ten animals. Three groups received intraperitoneal Cd²⁺ (0.25, 0.5 and 1 mg/kg, respectively) dissolved in saline twice a week for 3 months. The control group received only saline (0.3 ml). At the end of 3 months, the urinary bladders were surgically removed and a strip of detrusor was prepared from each bladder. An atomic absorption device and the standard addition method were used to determine blood levels of Cd²⁺ and the Cd²⁺ levels of the remaining parts of each bladder. The responses of the detrusor strips were studied in organ chambers. The tissues were first treated with ACh and then with EFS. The responses were recorded by isotonic transducers. The tissue Cd²⁺ levels were significantly increased in the Cd²⁺ treated rats in a dose-dependent manner except in the 0.25 mg/kg Cd²⁺ treated group. ACh-induced contractions were significantly attenuated only in the 1 mg/kg Cd²⁺ treated rats. The contractions induced by EFS were significantly decreased in all of the Cd²⁺-treated groups, but there were no significant differences between the groups. This study showed that Cd²⁺ exposure for 3 months impairs neurogenic and myogenic contractile activity in the rat detrusor muscle. This action seems to be at least partly due to an inhibition of the cholinergic muscarinic system. This may have clinical implications for people who are exposed to Cd²⁺.     

The latissimus dorsi bladder myoplasty to assist detrusor function

The objective of this study was to evaluate whether an innervated skeletal muscle might augment detrusor function. In four dogs we performed the latissimus dorsi myoplasty, a transfer of the latissimus muscle as an innervated free flap wrapped around the bladder. Stimulation of the latissimus dorsi free flap initially achieved an average bladder pressure of 45.8 ± 8.41 cm H₂O, sufficient for partial evacuation. After 4 months the muscle generated a maximal pressure of 82 cm H₂O, resulting in an evacuation of 27.7%. For selected patients, the latissimus dorsi bladder myoplasty may provide an alternative to intermittent catheterization in the future. Received: 14 March 1997 / Accepted: 12 January 1998     

The impact of detrusor overactivity on bladder function in younger and older women

PURPOSE: We examined the relationship of DO and aging, and bladder function in female volunteers. MATERIALS AND METHODS: We recruited 85 cognitively competent, fully functional female volunteers who were 22 to 90 years old (median age 54) with and without symptoms suggestive of DO. Comprehensive assessment included a bladder diary, uroflowmetry and videourodynamics. We examined predefined urodynamic and diary variables for associations with DO and age, summarizing results in the 3 subgroups no DO, intermediate DO and clinically relevant DO. RESULTS: Compared to women without DO those with DO showed a decrease in maximum cystometric capacity (558 vs 448 ml), mean daytime voided volume (260 vs 175 ml) and volume at strong desire to void (363 vs 283 ml) but an increase in maximum isovolumetric pressure (41 vs 64 cm H2O) and maximum detrusor pressure during involuntary contraction (intermediate and relevant DO 22 and 37 cm H2O, respectively). The positive association between increased detrusor contraction strength and DO was present at younger ages but absent in older subjects. Maximum urethral closure pressure and detrusor contraction strength decreased significantly with age. CONCLUSIONS: From young adulthood to old age DO appears to affect bladder function parameters. It is associated with decreased bladder capacity and increased bladder sensation. Moreover, in younger adults DO is also associated with increased detrusor contraction strength, which is an association not seen in older individuals. This age associated loss of muscle function may be related to sarcopenia, implying that different treatments may be appropriate in older adults.     

Cystometric studies of detrusor function after prostatectomy and transurethral electrosurgery

The detrusor function was studied by cystotonometry in 50 cases of adenomatous disease, prior to and after surgical removal of the obstacle situated at the neck of the bladder. From the results it emerges that the chances for an adequate surgical restoration of detrusor function depend on the radicality of the intervention rather than on its type. The postoperative period required for normalization of bladder function averages 3 months. Palliative transurethral resection holds no promise for any significant functional improvement.     

Effects of trimebutine and metoclopramide on colonic motility in the guinea pig

The effects of trimebutine (2-dimethylamino-2-phenylbutyl-3, 4, 5-trimethoxy benzoate hydrogen maleate) and metoclopramide (N-diethylaminoethyl-2-methoxy-4-amino-5-chlorobenzamide) on propulsive activity of the isolated segmental colon, and on longitudinal and circular muscle layers of colon in guinea-pig were investigated. Trimebutine in doses up to 10(-7) g/ml slightly stimulated propulsive activity, but in doses as high as 10(-7) g/ml inhibited it. However, metoclopramide (10(-7)-10(-5) g/ml) stimulated propulsive activity in a dose dependent manner. Neostigmine-stimulated propulsive activity was inhibited by trimebutine (10(-6) g/ml) but potentiated by metoclopramide (10(-5) g/ml). Trimebutine (10(-8)-10(-5) g/ml) contracted circular muscle layer in a dose dependent manner, and contracted longitudinal muscle layer in doses up to 10(-7) g/ml, but in doses as high as 10(-7) g/ml relaxed it. While, metoclopramide (10(-8)-10(-5) g/ml) contracted both muscle layers. These results indicate that, at high doses, trimebutine-induced inhibition of propulsive activity may depend on a relaxation of longitudinal muscle, and at low doses, trimebutine-induced stimulation of propulsive activity may depend on a contraction of longitudinal muscle which was partly inhibited by atropine (10(-6) g/ml), though metoclopramide at low doses had little effect on propulsive activity.     

Energetics of detrusor contraction: Effects of outlet obstruction

Previous studies demonstrated that the ability of the urinary bladder to empty was impaired after mild outlet obstruction. One contributing factor may be the derangement of intracellular energy metabolism. The primary objective of the current study is to examine the energentics of detrusor contraction in normal and obstructed rabbit urinary bladders. Mild bladder outlet obstruction was induced in male rabbits; after 2 weeks of partial outlet obstruction, three muscle strips were isolated from the bladder body of each obstructed and control rabbit. One of these strips was frozen at unstimulated state, while the remaining two strips were stimulated with 500 m?M bethanechol and frozen separately either at maximal phasic (peak) contraction or during plateau (tonic) contraction. Tissue content of adenine nucleotides (ATP, ADP, AMP), NAD (nicotinamide adenine dinucleotide), creatine, and creatine phosphate were determined using reverse phase high performance liquid chromatography (HPLC). The results can be summarized as follows: 1) The tissue content of creatine phosphate of the unstimulated control bladder was significantly higher than in the obstructed bladders. The tissue content of all other compounds were similar. 2) In the normal bladder strips, bethanechol stimulation induced a significant net decrease only in the tissue content of creatine phosphate during the plateau phase of contraction. 3) In the obstructed bladder strips, bethanechol stimulation induced a decrease in both ATP and creatine phosphate during the plateau phase of the response. The decrease in creatine phosphate was of a significantly greater magnitude than the decrease of creatine phosphate observed in normal strips. In addition, AMP content was significantly increased during both peak and plateau contraction. These observations show that mild bladder outlet obstruction results in changes in the energy metabolism of detrusor contraction, which indicates that the obstructed bladder is unable to maintain proper tissue levels of high energy phosphates which are necessary for adequate detrusor contraction.