Ethanol did not affect resting tension but acetaldehyde and ethanol suppressed bladder muscle contractions. However, direct acetaldehyde-stimulation may release histamine and enhance contractility. This suggests that chronic alcoholism rather than acute intoxication is more likely to provoke urinary retention.

Ethanol has various effects on male sexual activity under the influence of direct and indirect, in acute and chronic alcohol ingestion. However, whether acetaldehyde, a principal metabolite of ethanol, may affect penile erection directly has still not been elucidated. This present study was, therefore, designed to clarify the pharmacologic effects of the acetaldehyde on corpus cavernosal smooth muscle. Corpus cavernosal strips were prepared from rabbit penises. Isometric tension changes of rabbit corpus cavernosal strips to various drugs and electrical field stimulation (EFS) in an organ chamber were recorded with a pressure transducer after active muscle tone had been induced by phenylephrine (10(-5) mol/L). At the concentrations employed, acetaldehyde had no effect on the pH of the bathing medium. Acetaldehyde in each concentration did not significantly affect resting tone of the smooth muscle during 30 min incubation. Acetaldehyde suppressed contractility induced by phenylephrine and KCI at 10(-4) mol/L, and relaxation induced by EFS and bethanechol at 10(-3) mol/L and 10(-4) mol/L respectively, but acetaldehyde enhanced relaxation induced by ATP at high acetaldehyde level. Sodium nitroprusside-induced relaxation was not affected at any employed acetaldehyde concentration. This suggests that increasing the acetaldehyde level may contribute to male erectile dysfunction mainly by the inhibition of nitric oxide formation.

Background : A simple and non-invasive methods for the diagnosis of transitional cell carcinoma of the bladder are needed for the prevention of invasive tumor. A proteomic technology has recently been developed to facilitate protein profiling of biological mixtures. We tried to detect the marker proteins by proteomic approach during the initiation stages on N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder carcinogenesis in rats. Methods : Ten rats in group A were given 0.05% BBN in drinking water for 12 weeks. Other 10 rats in group B with 10 rats were designated as a control group and were not given BBN. Whole urinary bladders of all rats were excised at 12 weeks from the beginning of the experiment. Conventional proteomics was performed with high resolution 2-dimension gel electrophoresis followed by computational image analysis and protein identification using mass spectrometry. Results : A comparison of urinary bladder hyperplasia tissue with control tissue showed that five proteins; actin γ 2 propeptide, cytokeratin-20 (CK-20), proapolipoprotein, α 2 actin ( α -cardiac actin) and heat shock 27 kDa protein-1 were over-expressed in hyperplastic tissues. Three proteins; transcription factor myocardin, seminal vesicle secretory protein VI (SVS-VI) precursor and hypothetical protein RMT-7 were under-expressed in hyperplastic tissues. Conclusion : In our animal mode, BBN-induced urinary bladder mucosal hyperplasia resulted in an increase in the expression of five proteins and a decrease in the expression of three proteins. Of these, CK-20 and SVS-VI seem to be of particular interest. However other method such as Western blotting seems to be needed for confirmation of these proteins and more information on human bladder tissue is needed for clinical application.

We investigated the pathophysiological mechanism by proteomic approach as a possible tool to detect the marker proteins to develop lower urinary tract symptoms following bladder outlet obstruction (BOO). Rats were randomized into 3 groups; control, sham operation and BOO groups. BOO group was divided into 1, 3, and 5 day-group. Conventional proteomics was performed with high resolution 2-D gel electrophoresis followed by computational image analysis and protein identification using mass spectrometry using rat urinary bladders. A comparison of bladder of BOO group with control bladder showed that three proteins of optineurin, thioredoxin and preprohaptoglobin were over-expressed in the bladder of BOO group. In addition, four proteins, such as peroxiredoxin 2, transgelin, hippocampal cholinergic neurostimulating peptide (HCNP) and beta-galactoside-binding lectin, were under-expressed in the bladder of BOO group. These data supported that down-regulation of HCNP might make detrusor muscle be supersensitive to acetylcholine, up-regulation of optineurin means the protection of nerve injury, and down-regulation of transgelin means the decreased contractility of detrusor muscle. Beside these proteins, other proteins are related to oxidative stress or have a nonspecific function in this study. However more information is needed in human bladder tissue for clinical usage.

Purpose: One of the most serious complications of benign prostatic hyperplasia (BPH) is acute urinary retention (AUR). Up to now, many papers have evaluated the short term treatment of patients with AUR that is due to BPH. Therefore, we evaluated the long term follow-up of BPH patients with AUR. Materials and Methods: 154 BPH patients with AUR were divided into two groups. One group was considered to be the failure cases of urethral catheter removal, and this group (55 patients) had undergone immediately transurethral resection of prostate (TURP). The other group was considered to be the successful cases of urethral catheter removal. The latter group was divided into 3 groups: the -blocker group, the -blocker with 5 -reductase inhibitor group and the suprapubic cystostomy with medical treatment group. We evaluated the long term follow-up of these groups and the changes of treatment for 1 month, 3 months, 6 months and 12 months. Results: The mean volume of the prostate was 54.2ml. When the patients were admitted to the hospital due to AUR, 53% of the patients had previously experienced AUR, and the mean number of previous AUR episodes were 1.4 times. The initial management of AUR due to BPH was urethral catheter indwelling with medical treatment. If the catheter removal failed, TURP was perfomed (35%) and when successful, medical treatment was then done. Conclusions: The primary management of AUR due to BPH is urethral catheter indwelling with medical treatment ( -blocker). However, if the patients have a large size prostate, we should first consider hormone treatment (5 -reductase inhibitor) rather than surgical treatment. The management methods of some patients were changed during the follow-up. Therefore, when following up these cases, we should be careful to prevent the recurrence of AUR and to allow self-voiding.