Diagnosis of Urinary Bladder Dysfunction in Diabetes Mellitus

Bradley, William E.

doi:10.7326/0003-4819-92-2-323

Cited by 105 publications

(52 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The finding that the EFS-evoked cholinergic response generated significantly greater tension in diabetic detrusor compared to the control is unexpected, as well as puzzling, since clinical diabetes mellitus is frequently associated with a 'failing' detrusor function (Fagerberg et al, 1967;Kahan et al, 1970;Buck et al, 1974;Bradley, 1980;Ellenberg, 1980). In theory, the enhanced nerve-mediated cholinergic response of the diabetic detrusor must have originated in either an augmented sensitivity of the detrusor to released ACh, or to an augmented ACh release, or to a combination of both of these factors.…”

Section: Discussionmentioning

confidence: 99%

The effect of streptozotocin‐induced diabetes on cholinergic motor transmission in the rat urinary bladder

Luheshi¹,

Zar²

1991

British J Pharmacology

View full text Add to dashboard Cite

1The effect of streptozotocin (STZ)-induced diabetes on cholinergic motor transmission in the rat urinary bladder was investigated by recording contractile activity of detrusor strips in vitro. 2 The Ca2+-channel antagonist, nifedipine, was found to be more effective in blocking the noncholinergic motor transmission than P2-purinoceptor desensitization by ocxJ-methylene ATP. 3 The neurogenic contractile responses to electrical field stimulation in the presence of nifedipine (cholinergic) were larger in the diabetic detrusor than in the non-diabetic controls. The potentiation of the cholinergic transmission was more evident at higher frequencies. 4 Concentration-response curves for acetylcholine were identical in detrusors from diabetic and nondiabetic animals, thus excluding a postsynaptic supersensitivity to acetylcholine being responsible for the potentiation of cholinergic motor transmission. 5 It is concluded that the potentiation of cholinergic motor transmission is due to enhanced release of acetylcholine in diabetic detrusor. Possible reasons for this enhancement are discussed in relation to diabetes.

show abstract

Section: Discussionmentioning

confidence: 99%

The effect of streptozotocin‐induced diabetes on cholinergic motor transmission in the rat urinary bladder

Luheshi¹,

Zar²

1991

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Bladder underactivity, which includes decreased contractility, increased capacity, increased residual urine, and impaired sensation, is characteristic of the bladder dysfunction seen in the majority of patients with diabetes [32,33].…”

Section: Discussionmentioning

confidence: 99%

Does diabetes affect the intensity of staining of interstitial cells and neuronal tissue in the bladder, prostate and urethra of rabbits?

et al. 2010

View full text Add to dashboard Cite

AbstractWe compared the intensity of staining of interstitial cells (ICs) and neural tissue in the lower urinary tract of rabbits with diabetes with the intensity in normal subjects. Diabetes was induced by injecting alloxane (65mg/kg) in adult male rabbits. After 3 days, rabbits with a blood glucose level >300 mg/dL were considered to have diabetes. After 8 weeks, the rabbits were killed, and tissue specimens from the bladder, prostate and urethra were obtained. ICs were stained with anti-human CD117 (c-kit) rabbit polyclonal antibody, and neural tissue was stained with synaptophysin. The streptavidin-biotin method was used for immunohistochemical staining. The intensity of c-kit and synaptophysin staining were scored as negative (0), weak (+), moderate (++), and strong (+++). Staining intensity of ICs and neural tissue was assessed and compared in tissues obtained from rabbits with diabetes (n=8) and from control subjects (n=7). Although staining intensity of both ICs and neural tissue was found to be significantly decreased in the bladder tissue of rabbits with diabetes compared to that in the control group (p=0.0001 [ICs] and p=0.021 [neural tissue]), no significant differences in staining intensity of ICs and neural tissue in the urethra and in the prostate was found when rabbits with diabetes were compared to the control group. Diabetes may cause dysfunction of the lower urinary tract, particularly in the urinary bladder, as shown by the staining intensity of ICs and neural tissue.

show abstract

“…Bu durum inkomplet mesane boşalmasına, artmış rezidü idrara, azalmış üriner pik akım oranına, mesane aşırı distansiyonuna ve üriner retansiyona neden olmaktadır. Sonuç olarak internal ve eksternal sfinkterlerin denervasyonu sonucunda taşma (overflow) inkontinansı gelişir (11). Miksiyon sonrası rezidüel volumün 150 ml'den fazla olması nörojenik mesane için diyagnostiktir.…”

Section: Nörojenik Mesaneunclassified

Current Diagnosis and Treatment Approaches in Diabetic Autonomic Neuropathy

Araç¹

2017

Turk J Bioch

View full text Add to dashboard Cite

Diyabetik otonom nöropati, diyabetin en sık ve en sıkıntı verici komplikasyonudur. Otonom sinir sistemi (OSS) tutulumu genellikle diffuz olsa da, semptomlar tek bir hedef organ veya sistem ile sınırlı olabilir.Diyabetik otonom nöropatinin komplikasyonları mortalite ve morbiditede artışa, yaşam kalitesinde azalmaya ve diyabetik hastaların tedavi maliyetinde artışa sebep olmaktadır.Bu komplikasyonların patogenezindeki faktörler; metabolizmada değişme, vasküler yetersizlik, büyüme faktörlerinin trofizminde kayıp ve viseral ve kutanöz sinirlerde otoimmun destriksiyon olarak sıralanabilir. Diyabetik otonom nöropatinin komplikasyonları ve klinik manifestasyonları ile ilgili yayınlar mevcuttur. Gelecekte, hastalığın altında yatan patolojik sürecin daha iyi anlaşılması ile birlikte, tedaviler manifestasyona değil neden yönelik olabilir. Halen sürmekte olan ve otonom sinirlerin rejenerasyonunun indüklenebilir olduğu bir takım çalışmaların varlığı, diyabetik otonom nöropati hastalarının tedavisinde ümit vericidir. AbstractDiabetic autonomic neuropathy is the most common and troublesome complication of diabetes mellitus. Though involvement of the autonomic nervous system is generally diffuse, symptoms may be confined to a single target organ or organ system. Complications of diabetic autonomic neuropathy contribute greatly to the morbidity, mortality, and reduced quality of life of the person with diabetes and are the major source of increased costs of caring for the diabetic patient. Factors in the pathogenesis of these complications are altered metabolism, vascular insufficiency, loss of growth factor trophism, and autoimmune destruction of nerves in a visceral and cutaneous distribution. The clinical manifestations and the complications of diabetic autonomic neuropathy are reviewed. Future therapeutic strategies that are developed from a better understanding of the pathogenetic processes underlying this disorder can be directed at the cause rather than the manifestations. There are studies in progress that suggest that autonomic nerves can be induced to regenerate, and the future for patients with diabetic autonomic neuropathy is brighter.

show abstract

Diagnosis of Urinary Bladder Dysfunction in Diabetes Mellitus

Cited by 105 publications

References 9 publications

The effect of streptozotocin‐induced diabetes on cholinergic motor transmission in the rat urinary bladder

The effect of streptozotocin‐induced diabetes on cholinergic motor transmission in the rat urinary bladder

Does diabetes affect the intensity of staining of interstitial cells and neuronal tissue in the bladder, prostate and urethra of rabbits?

Current Diagnosis and Treatment Approaches in Diabetic Autonomic Neuropathy

Contact Info

Product

Resources

About