Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isoprostane 8-epi PGF2alpha is a product of oxidative stress that causes potent smooth muscle contraction. Its production increases in conditions associated with oxidative stress such as in diabetes, smoking, and aging. The aim was to study whether the urinary bladder synthesizes isoprostane 8-epi PGF2alpha and releases to the urine and whether isoprostane 8-epi PGF2alpha causes bladder smooth muscle contraction. Urine samples were obtained transurethrally from 12 male New Zealand white rabbits for measurement of isoprostane 8-epi PGF2alpha levels. To examine whether bladder synthesizes isoprostane 8-epi PGF2alpha, both ureters were ligated, then the bladder was washed 5 times by filling and emptying with normal saline. Bladder was refilled with normal saline, and at 5 minutes a bladder washout sample was taken. After this, the bladder was contracted by nerve stimulation periodically for 30 minutes, and then another washout sample was taken. Strips of bladder tissues were processed for study of isoprostane 8-epi PGF2alpha production in tissue culture chambers and for isometric tension measurements in the organ bath. Enzyme immunoassay (EIA) revealed a remarkable amount of isoprostane 8-epi PGF2alpha in the rabbit urine. EIA of washout samples showed that the bladder synthesizes isoprostane 8-epi PGF2alpha and its production increases with nerve stimulation-induced contractions. EIA of samples from the tissue culture media showed that bladder strips synthesize isoprostane 8-epi PGF2alpha in vitro. Electrical field stimulation (EFS) significantly increased the synthesis and release of isoprostane 8-epi PGF2alpha by the bladder strips. In the organ bath, isoprostane 8-epi PGF2alpha caused concentration-dependent contraction of bladder tissue. While the threshold contraction required smaller concentration of isoprostane 8-epi PGF2alpha (3 nmol) than carbachol (10 nmol), the amplitude of contraction to carbachol was greater than isoprostane 8-epi PGF2alpha. Our studies show that the rabbit bladder synthesizes isoprostane 8-epi PGF2alpha and releases it to the urine. Production of isoprostane 8-epi PGF2alpha in the bladder increases with nerve stimulation-induced contraction. Exogenous isoprostane 8-epi PGF2alpha causes significant bladder smooth muscle contraction. Our findings necessitate further studies to evaluate the possible role of oxidative stress and increased isoprostane 8-epi PGF2alpha production in bladder dysfunction. Neurourol. Urodynam. 19:43-51, 2000.
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PMID:Isoprostane 8-epi PGF2alpha, a product of oxidative stress, is synthesized in the bladder and causes detrusor smooth muscle contraction. 1060 47

The underlying risk factors, presenting features, and outcome of 22 children with sacral agenesis and associated neuropathic bladder were studied retrospectively. The age of children at presentation was bimodally distributed, with peaks below 1 year and between 4 and 5 years of age. Ten patients presented after 1 year. The oldest was diagnosed at 12 years of age. In 12 children there was maternal diabetes, orthopaedic anomalies in 14, skin defects in 11, and anorectal/tracheooesophageal anomalies in three. Most children had persistent dribbling of urine on presentation associated with frequency, urgency, recurrent urinary tract infections, failure to respond to medication, and/or constipation. Twenty-one children had abnormal neurology in the lower limbs. Videourodynamics showed neuropathic vesicourethral dysfunction in all children and vesicoureteric reflux in 10. Nineteen had a history of urinary tract infections. Seven had renal scarring, with renal impairment in three at presentation. Clean intermittent catheterization was recommended for 20 of the children. Bladder or bowel surgery has been carried out in seven and neurosurgery performed in two. Twenty of the 22 children underwent operative procedures. Ten operations were performed before sacral agenesis was diagnosed. Over a third of the children have required psychological support. The combination of urinary symptomatology and any of the above risk factors should give rise to a high level of suspicion and low threshold to perform investigations to exclude sacral agenesis. All these children have abnormal bladder and urethral function which not only causes incontinence but puts the kidneys at risk. Early detection allows effective multidisciplinary input specifically aimed at continence, preservation of renal function, and adequate psychological support.
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PMID:Presentation and outcome of sacral agenesis: 20 years' experience. 1103 61

Urinary bladder dysfunction and remodeling are well-recognized phenomena in diabetes but detailed assessments of tissue morphological changes have not been conducted. We studied time-dependent morphological changes in bladders from diabetic rats (streptozotocin model) and evaluated the usefulness of automated digital imaging technology as an unbiased, reproducible, and convenient method for the bladder morphometric analysis. Urinary bladders were isolated from diabetic (3 days, 2 weeks or 5 weeks after single injection of streptozotocin, 65 mg/kg) or control rats (0 or 5 weeks) and were processed for histochemical evaluations (hematoxylin/eosin and Mason's trichrome staining). Digital image analysis was used to quantify equatorial cross-sectional areas of bladder tissue and lumen, as well as relative prevalence of the three primary tissue components viz. smooth muscle, urothelium, and extracellular matrix. Digital imaging and color segmentation provided reliable and unbiased evaluations of the bladder tissue sections. Progressive increases in total bladder tissue and lumen area were observed in the diabetic animals relative to controls (p<0.05), demonstrating classic hypertrophy and dilation. Prevalence of smooth muscle and urothelium (% of total tissue) both increased significantly, but collagen content decreased. Average bladder wall thickness and urothelium thickness were unchanged. Bladder remodeling during experimental diabetes is associated with time-dependent chamber dilation and increased tissue mass. Changes in bladder wall composition also occurred in a time-dependent manner, most notably increased smooth muscle and urothelium and decreased collagen prevalence. Furthermore, automated digital imaging technologies provide an unbiased, reproducible, and convenient method for detailed morphometric analysis of bladder tissues.
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PMID:Time-dependent urinary bladder remodeling in the streptozotocin-induced diabetic rat model. 1204 35

The aim of this study is to determine the early effects of partial outflow obstruction (POO) on the detrusor contractility of diabetic (DM) and non-diabetic rats. A total of 67 adult female Wistar rats with average weight of 214+/-3.1 g were randomized into five groups as control ( n=6), sham operated ( n=6), obstructed ( n=18), DM ( n=19), and DM with obstruction ( n=18). Intraperitoneal injection of 60 mg/kg streptozotocin was performed to achieve DM. Partial bladder neck obstruction was created surgically by ligating the urethra around a 3F feeding tube. Bladder strips were obtained and inspected on days 3, 7, and 14 of both the diabetic period and POO. Mean detrusor weights were measured and the maximal contractile responses to carbachol (Car), adenosine 5'-triphosphate (ATP), substance P (SP) and electrical field stimulation (EFS) of detrusor strips in all groups were studied in vitro. After 14 days of obstruction, no remarkable difference was observed between the maximal contractile responses to Car and SP of strips from obstructed-only (POO) and diabetic-obstructed (DM-POO) rats compared to the control group. The responses to EFS and ATP in the POO rats were significantly lower than the controls ( P<0.01, P<0.01, respectively). In the DM-POO group however, the responses were significantly better than the POO group, reaching almost similar levels with the controls. The contractile responses of DM-POO rats were higher than the POO group but lower than the DM group. Better contractile responses of the rats with DM-POO than POO group can be explained by the early enhancing effects of DM on detrusor contractility. In early DM+POO period, the negative effects of POO on detrusor muscle contractility is masked by diabetes mellitus.
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PMID:The early effects of partial outflow obstruction on contractile properties of diabetic and non-diabetic rat bladder. 1211 Nov 81

PURPOSE It has been proposed that a deficiency in the axonal transport of nerve growth factor (NGF) may have an important role in inducing diabetic neuropathy, which contributes to diabetic cystopathy. Therefore, in streptozotocin (Sigma Chemical Co., St. Louis, Missouri) induced diabetic rats we investigated the relationship of bladder function with NGF levels in the bladder and lumbosacral dorsal root ganglia, which contain afferent neurons innervating the bladder. MATERIALS AND METHODS At 6 and 12 weeks after the induction of diabetes with streptozotocin (65 mg./kg. intraperitoneally) the effects of diabetes on Adelta afferent fiber dependent, conscious voiding were evaluated by metabolic cage measurements and awake cystometry. The effects of diabetes on C-fiber mediated bladder nociceptive responses were also investigated by cystometry with intravesical instillation of 0.25% acetic acid in the rats under urethane anesthesia. NGF levels in the bladder and L6 to S1 dorsal root ganglia were measured by enzyme-linked immunosorbent assay 3, 6, 9 and 12 weeks after streptozotocin injection. RESULTS In diabetic rats NGF levels in the bladder and L6 to S1 dorsal root ganglia were significantly decreased 12 weeks after streptozotocin injection (p <0.01). In cystometry and metabolic cage studies bladder capacity and post-void residual volume were significantly increased 12 weeks after streptozotocin injection (p <0.01). Bladder nociceptive responses revealed by a reduction in inter-contraction intervals after acetic acid infusion were significantly decreased in a time dependent manner 12 weeks after streptozotocin injection.CONCLUSIONS Rats with streptozotocin induced diabetes mellitus showed a significant time dependent decrease in NGF levels in the bladder and L6 to S1 dorsal root ganglia that was associated with voiding dysfunction attributable to defects in Adelta and C-fiber bladder afferents. Therefore, reduced production of NGF in the bladder and/or impaired transport of NGF to L6 to S1 dorsal root ganglia, which contain bladder afferent neurons, may be an important mechanism inducing diabetic cystopathy.
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PMID:Diabetic cystopathy correlates with a long-term decrease in nerve growth factor levels in the bladder and lumbosacral dorsal root Ganglia. 1218 78

Bladder overactivity (OAB) is a common disease with a socioeconomic impact comparable to diabetes mellitus. As life expectancy rises in industrialized countries the importance of OAB will further increase. The International Continence Society (ICS) recently reported a modified terminology for lower urinary tract function and established the symptom-based term OAB. The etiology of OAB comprises neurogenic and non-neurogenic detrusor hyperactivity as well as detrusor hypersensitivity. Neurogenic detrusor hyperactivity may be caused by insufficient cortical inhibition, degenerative neuropathies, and spinal cord lesions, whereas bladder aging, bladder outlet obstruction, and chronic bladder irritation (UTI, stones, tumors) are possible causes for non-neurogenic detrusor hyperactivity. Since most epidemiologic surveys focus on urge incontinence without considering urgency frequency without incontinence, epidemiologic data concerning OAB are rare. Two recently published multinational prevalence studies from Europe and Asia show different prevalence values [Europe: 15.6% (men), 17.4% (women); Asia: 53.1%(women)], which may be due to methodological differences. Both studies report an increase of OAB prevalence corresponding with age. The cumulative incidence of OAB is rising faster in aging males than in aging females. Two-thirds of the European and one-fourth of the Asian individuals affected by OAB complained about impaired quality of life, but only 60% of the European and 21% of the Asian sufferers have talked to a doctor or sought treatment. One out of four patients visiting their health care professional for OAB symptoms is currently under medication. To avoid high treatment costs and side effects, pharmacotherapy (e.g., antimuscarinics) should only be given after detailed diagnostic evaluation.
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PMID:[Epidemiology and etiology of overactive bladder]. 1285 68

Bladder dysfunction can result from pathological changes in the bladder itself, of its central neurological regulation, (BPS), or of non-urological diseases such as diabetes or heart failure. Medication-induced bladder dysfunction can mostly be treated by simple changes in the pharmacological therapy. Bladder dysfunction can be induced pharmacologically by activating or inhibitory influences on adrenergic, sympathetic, beta-receptor-induced relaxation of the detrusor, alpha-receptor-induced contraction of the bladder neck, or cholinergic, parasympathetic, muscarinic receptor-induced contraction of the detrusor. Diuretics can increase urine production, thus possibly leading to incontinence. If incontinence occurs in patients, treatment should be stopped if possible and additional pharmacological therapy should not be started before medication-induced bladder dysfunction is excluded.
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PMID:[The medication-induced dysfunction of the urinary bladder]. 1466 86

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.
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PMID:Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes. 1568 44

Urinary bladder dysfunction is a common complication in diabetes, but the mechanisms involved are undefined and treatment options are limited. Murine models provide opportunities to utilize transgenic technologies for bladder research and here we investigate the functional, structural and neuronal aspects of the bladder in a mouse model of type-1 diabetes. Mice were injected with streptozotocin (150 mg/kg) or vehicle and studied at 5 weeks. Increases in blood glucose and total urine output were observed. In vitro cystometry showed a 2-fold increase in bladder capacity and compliance and decreased intravesical plateau pressure in diabetics versus controls. Bladder structure and composition were evaluated by digital imaging; region-specific changes included increased smooth muscle and urothelium and no change in collagen content. Alterations in cholinergic, adrenergic and nitric oxide-related functional responsiveness were also observed. The prevalence of cholinergic and adrenergic neuronal tracts was determined by immunohistochemistry: decreased vesicular acetylcholine transferase was observed in smooth muscle, whereas tyrosine hydroxylase was increased in the lamina propria, demonstrating a 'neuronal remodeling' shift toward pro-relaxant neuronal pathways. These studies demonstrate that this mouse model of diabetes exhibits important features of urinary bladder remodeling that are similar to the findings in humans and other animal models and will therefore be useful for further mechanistic investigations.
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PMID:Functional, structural, and neuronal alterations in urinary bladder during diabetes: investigations of a mouse model. 1571 7

The urinary bladder of four dogs with emphysematous cystitis was assessed radiographically. Ultrasonography was also performed using a 7.5-MHz microconvex probe in dorsal recumbency and in a standing position. Ultrasonographically there were bright echoes and reverberations typical of gas in all dogs. This was entrapped in the bladder wall as it appeared in the same location in recumbent and standing positions. Bladder size was reduced and bladder content was echogenic in all dogs. In only one out of the four dogs was a gas stripe seen in the bladder on radiographs. Proteus mirabilis was isolated from the urine of all patients. Diabetes was ruled out on the basis of urine and blood analysis. A small amount of gas can be difficult to detect on radiographs. Ultrasonography appears to be a more sensitive technique for detection of gas within the bladder at an early stage of emphysematous cystitis. Prevalence of emphysematous cystitis may be underestimated if only radiographs are made.
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PMID:Radiographic and ultrasonographic findings of emphysematous cystitis in four nondiabetic female dogs. 1642 92


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