Detrusor overactivity of the conscious rats was induced by cold environmental stress. A portion of the cold-stress detrusor overactivity might be mediated by RTX-sensitive neurological pathway. The cold-stress model would be useful to investigate lower urinary tract functions.
Aims: We determined if Gosha-jinki-gan, a traditional Chinese herbal mixture, reduced the presence of the tachykinins neurokinin A, neurokinin B, and substance P, as well as the transient receptor potential vanilloid 1 (TRPV1) and P2X3 purine receptors that are functionally associated with C fibers in the urinary bladder. Methods: Thirty-six female rats were fed with either a standard diet or one supplemented with 1.08% Gosha-jinki-gan. After 4 weeks, the urinary bladders were instilled with either saline or 0.1% acetic acid. After 30 minutes, the bladders were removed and expression of the tachykinins and the TRPV1 and P2X3 receptors was determined by immunohistochemistry and mRNA expression. Results: In rats fed with the standard diet, the tachykinins and the TRPV1 and P2X3 receptors expressed nearby or within urothelium of the acetic acid-treated rats increased compared with the saline-instilled rats. In rats pretreated with Gosha-jinki-gan, the tachykinins and the TRPV1 and P2X3 receptors in the acetic acid-treated rats also increased compared with the saline-instilled rats. However, with the instillation of acetic acid, the tachykinins and the TRPV1 and P2X3 receptors of Gosha-jinki-gan pretreated rats decreased compared with standard diet fed rats. The mRNA expression levels of neurokinin A, substance P, and the TRPV1 receptor in acetic acid-treated Gosha-jinki-gan pretreated rats were lower than that in acetic acid-treated standard diet fed rats. Gosha-jinki-gan did not destroy nerve fibers within the bladders. Conclusions: Gosha-jinki-gan partially reduced the tachykinins and TRPV1 and P2X3 purine receptors without destroying the nerve fibers.(247/250 words) 3
In SHRs, THC-002 reduced the bladder expression of tachykinins and P2X3 and TRPV1 receptors, and inhibited ATP-induced detrusor overactivity. These effects may explain part of its beneficial effects on LUTS.
ABSTRACT:This study was performed to investigate the effects of goshajinkigan, a traditional Chinese herbal mixture, in conscious rats undergoing continuous cystometry.Systemic resiniferatoxin (RTX) pretreatment can block resiniferatoxin-sensitive (C-fiber) nerve-mediated bladder overactivity, such as that induced by intravesical administration of acetic acid. The effects of pretreatment with goshajinkigan and resiniferatoxin (RTX) alone or in combination on acetic acid-induced bladder overactivity in conscious rats were also compared. Female SD rats were divided into 4 groups. Group (1), (3) received normal food for 4 weeks, while groups (2) and (4) received goshajinkigan (0.09 g/kg/day) during the same period. Two days after bladder catheterization, groups (3) and (4) received RTX (0.3 mg/kg) injection, while groups (1) and (2) received vehicle alone. Cystometric investigations were performed on all animals 24 h after RTX or vehicle injection. The effects of intravesical instillation of acetic acid (pH=4.0) were compared with those of intravesical saline. Goshajinkigan significantly increased threshold pressure, voiding interval, micturition volume, and bladder capacity. Intravesical instillation of acetic acid induced bladder overactivity in both normal rats and in those pretreated with goshajinkigan. However, the effects of acetic acid on voiding interval and micturition volume were significantly different between rats given normal diet and those pretreated with goshajinkigan. The effect of acetic acid was not different between goshajinkigan-and RTX-pretreated rats. The results of the present study indicated that goshajinkigan increases voiding interval, micturition volume, and bladder capacity, and pretreatment partially blocks the bladder overactivity induced by intravesical administration of acetic acid in rats.
Aim : In the present study, we evaluated the relationships between prostate-specific antigen (PSA) level and bone metastasis, between Gleason sum and bone metastasis, and between clinical T stage and bone metastasis in Japanese patients. Methods : Between November 1998 and June 2004, we performed ultrasound-guided biopsies on 709 patients (mean age: 70.5 years, range: 39-90). Prostate cancer was detected in 339 patients (47.8%), 297 (87.6%) of whom underwent a radionuclide bone scan. In close collaboration with orthopedists, bone computed tomography scans, bone magnetic resonance imaging and/or plain rentogenograms were performed for cases that were difficult to diagnose as bone metastasis through radionuclide bone scans only. Results : We detected 61 (20.6%) bone metastasis cases in 296 patients. A simple linear regression analysis between log[PSA] and bone metastasis ( n = 296) produced a significant relationship ( P < 0.05). When we set the cut-off PSA value for the indication for a bone scan at 15 ng/mL, the possibility of bone metastasis was 10%. However, from our experience, there was no bone metastasis in the patients whose Gleason sums were less than five, and in the patients whose Gleason sum were five or more, and the PSA levels were less than 15, there was no bone metastasis. The rate of bone metastasis increased with the increase of PSA level. In the clinical T 1 -T 2 stage cases, there were significant higher PSA levels in the cases with bone metastasis. In the T 1 -T 2 patients whose PSA levels were less than 16, there was no bone metastasis. Conclusions : From the analysis of PSA, Gleason sum and clinical T stage, we suggest that bone scan is unnecessary for patients whose PSA level is less than 15 ng/mL or Gleason sum is less than five.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.