Electroacupuncture protects against bladder dysfunction induced by acute urinary retention via TRPV1/ATP signaling pathway: An animal and human research study.

Electroacupuncture (EA) can protect against acute urinary retention (AUR); however, the underlying mechanism remains unclear. Non-vesicular ATP release mediated by transient receptor potential (TRP) channels were identified as a key contributor to signaling in urothelial cells. In this study, the AUR model was established by urethral outlet obstruction in female Sprague-Dawley rats. EA was performed at SP6 and BL32 for 0.5 h prior to induction of AUR. EA reduced TRPV1 expression and urinary ATP concentrations in rat bladder, decreased the peak intravesical pressure during AUR, and attenuated abnormal voiding patterns and bladder pathological injury induced by AUR. Besides, 179 patients who experienced postoperative urinary retention were recruited and found that EA reduced urinary ATP concentrations and accelerated the recovery of spontaneous voiding. These observations indicate that EA exerts protection against AUR-induced bladder dysfunction by reducing urinary ATP concentrations through the regulation of TRPV1.

Molecular mechanisms of voiding dysfunction in a novel mouse model of acute urinary retention.

Acute urinary retention (AUR) is a common urological emergency and affects a significant patient population. The inability to eliminate urine may lead to permanent damage to the bladder's structure and functioning. However, we know little about the underlying molecular sequelae to the urine retention. To closely mirror the potential high pressures that patients with AUR could experience, we catheterized anesthetized female mice via the urethra and filled the bladder by pumping saline (25 µL/min) into the bladder lumen to 50 cm or 80 cm water pressure. A water column with designated height (50 or 80 cm) was then adjusted to maintain constant pressure in the bladder lumen for 30 minutes. Functional and morphological evaluations were performed from 0 to 24 hours after AUR treatment. Mice exhibited incontinence and overactivity with diminished voiding pressure. Significant injury was confirmed which revealed bladders with disrupted urothelial barrier, edematous lamina propria, and distorted muscle bundles. Bladder smooth muscle (BSM) from pressure-treated mice have significantly diminished contraction force, suggesting that bladder voiding dysfunction can be attributed to impaired BSM contractility. Indeed, dysregulation of acetylcholine and purinergic signaling pathways were demonstrated, indicating that reduced efficacy of these pathways contributes to impaired BSM contractility. Finally, altered expression of ß1-integrin and extracellular matrix mediated mechanotransduction pathways were detected, suggesting a profound remodeling process. These data demonstrated an easy to perform, quantifiable, and reproducible AUR mouse model, which mimics well the characteristics of human AUR patients, and our data generate new insights into the molecular mechanisms that occur following AUR.

Review of the Roles and Interaction of Androgen and Inflammation in Benign Prostatic Hyperplasia.

The lower urinary tract symptoms (LUTSs) and acute urinary retention (AUR) caused by benign prostatic hyperplasia (BPH) can seriously affect the quality of life of elderly men. Studies suggest that both androgens and inflammation greatly influence the occurrence and development of BPH in most patients. These two factors combined can also affect each other, leading to pathological changes in the stromal and epithelial tissue of the prostate transition zone in BPH patients. DHT in the prostate tissue of BPH patients may activate a chronic inflammatory response in the prostate, amplifying the expression of inflammatory factors and upregulating the proliferation ability of prostate tissue.

MicroRNAs as potential biomarkers to predict the risk of urinary retention following intradetrusor onabotulinumtoxin-A injection.

AIMS: MicroRNAs (miRs) control post-transcriptional gene expression, and this is relevant in understanding better chronic diseases and treatment outcomes. The role of miRs in the pathology and treatment outcomes of overactive bladder (OAB) is unknown. In this study, we assessed the differential expression of miRs in OAB patients responding with either normal or elevated post-void residual volumes (PVRs) ≥200 mL following intradetrusor injection of onabotulinumtoxin-A (onaBoNT-A). METHODS: Female OAB patients refractory to OAB drugs were consented for this study. Cystoscopic-guided punch bladder biopsy was obtained at the time of injection of onaBoNT-A 100 units. The expression of 13 miR species, selected for their known effect on neurotrophin expression and smooth muscle function, was measured. PVRs and urine nerve growth factor (NGF) levels were measured at baseline and at the follow-up visit. RESULTS: Fourteen patients with mean age of 66 years were consented. Of these patients, nine maintained PVRs <200 mL after onaBoNT-A injection to comprise the low PVR group. The other five patients with PVRs ≥200 mL comprised the high PVR group. The expression of miR221 and miR125b was upregulated by 11- and 2-fold, respectively, in patients who responded with low PVRs after onaBoNT-A (P < 0.05). Urine NGF levels at baseline were not different between the two groups. CONCLUSIONS: This study suggests that deficiency in the pretreatment expression of miR221 and miR125b may predispose OAB patients to high PVRs following intradetrusor onaBoNT-A. Additional studies are needed to better understand the role of miRs in OAB.

Effect of onabotulinum toxin type a intraprostatic injection on the outcome of benign prostatic hyperplasia patients refractory to medical therapy: a 2-year follow-up study / Efecto de la inyección intraprostática de Toxina botulínica tipo A en la evolución de los pacientes con Hiperplasia Prostática Benigna refractarios a tratamiento medico: Estudio de seguimiento a dos años

OBJECTIVES: To determine the outcome of Benign Prostatic Hyperplasia patients refractory to standard medical therapy and with significant comorbidities submitted to intraprostatic injection of onabotulinum toxin A. METHODS: Thirty-seven patients with symptomatic Benign Prostatic Hyperplasia refractory to medical therapy who were poor candidates for surgical treatment were enrolled. All patients voided spontaneously. They received one single transrectal application of 200 U of onabotulinum toxin A. All medical therapy was discontinued. The primary objective was to evaluate the percentage of patients that were still accepting to postpone the surgery at 2 years. As secondary objectives the variation of International Prostate Symptom Score and maximum urinary flow rate were also investigated. RESULTS: From the initial cohort, 2 patients developed severe cognitive impairment and eight patients abandoned the study and opted for surgery, due to acute urinary retention or lack of symptomatic improvement. Four patients were lost to follow-up. In the non-failure cohort, baseline International Prostate Symptom Score and Quality of Life and Postvoid Residual Volume decreased significantly and Maximum urinary flow rate increased significantly after injection. Prostate-Specific Antigen values showed no statistically significant variation. We did not find any statistically significant differences between the 2 cohorts regarding basal parameters. CONCLUSIONS: Intraprostatic onabotulinum toxin A injection can be an option for treatment of Benign Prostatic Hyperplasia/Lower Urinary Tract Symptoms refractory to medical treatment in poor surgical candidates, preventing surgery in at least two thirds of the patients. Side effects are limited to acute prostatitis

OBJETIVOS: Determinar la evolución de los pacientes con hiperplasia benigna de próstata refractarios al tratamiento médico estándar y con comorbilidad significativa sometidos a inyección intraprostática de toxina botulínica tipo A. MÉTODOS: Se incluyeron treinta y siete pacientes con HBP sintomática refractaria a tratamiento médico que eran malos candidatos para tratamiento quirúrgico. Todos los pacientes orinaban espontáneamente. Recibieron una única aplicación de 200 U de toxina botulínica A por vía transrectal. Se suspendió toda la medicación oral. El objetivo primario era evaluar el porcentaje de pacientes que a los dos años continuaban aceptando posponer la cirugía. Cómo objetivos secundarios también se investigaron las variaciones del IPSS (Índice internacional de síntomas prostáticos) y el flujo urinario máximo. RESULTADOS: De la cohorte inicial, 2 pacientes desarrollaron un empeoramiento cognitivo severo y ocho pacientes abandonaron el estudio y optaron por cirugía, por retención aguda de orina o falta de mejoría sintomática. Cuatro pacientes se perdieron en el seguimiento. En la cohorte que no fracasó, el IPSS basal, la calidad de vida y el volumen residual disminuyeron significativamente y el flujo urinario máximo aumentó de forma significativa después de la inyección. Los valores de PSA no mostraron una variación significativa. No encontramos diferencias estadísticamente significativas entre las dos cohortes en relación con los parámetros basales. CONCLUSIONES: La inyección intraprostática de toxina botulínica A puede ser una opción en el tratamiento de los STUI/HBP refractarios a tratamiento médico en malos candidatos para cirugía, evitando la operación en al menos dos tercios de los pacientes. Los efectos secundarios se limitan a prostatitis aguda

Quiste intrabdominal y retención crónica de orina / Abdominal cyst and chronic urinary retention

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Putting the past behind us: Social stress-induced urinary retention can be overcome.

INTRODUCTION: To study the pathophysiology of dysfunctional voiding, we have previously developed a model of stress-induced voiding dysfunction. We have shown that cyclosporine A (CsA), an inhibitor of the Ca(2+)-calmodulin complex, can prevent social stress-induced urinary retention. However, treatment with cyclosporine has not had an effect on the increase in the stress peptide corticotrophin-releasing factor (CRF) in Barrington's nucleus, which is involved in the micturition pathway. OBJECTIVE: We now investigate whether cyclosporine administered after stress can reverse the abnormal voiding phenotype, and whether it has effects on the bladder wall itself, or on the stress response within Barrington's nucleus. MATERIALS AND METHODS: Six-week old Swiss-Webster mice were exposed to aggressor males for 1 h a day, followed by 23 h of barrier separation. In a long-term trial, 1 month of stress was followed by single-cage housing for 6 months. In a separate CsA reversal trial, mice either received CsA in drinking water or had plain drinking water during 1 month of single-cage housing during recovery. Bladder contractile function was examined on a Guth myograph. Nuclear translocation of myocyte enhancing factor (MEF)-2 and NFAT (nuclear factor of activated T cells) in the bladder was assessed using electrophoretic mobility shift assays (EMSAs). The expression of CRF was determined in Barrington's nucleus using in situ hybridization. RESULTS: Voiding dysfunction persisted for up to 6 months after stress exposure while mice recovered in single-cage housing. In the CsA reversal trial, voiding patterns improved when they received CsA in water during single-cage housing following stress, whereas those that underwent single-cage housing alone had persistent abnormal voiding (Fig. A). There was no difference between CRF levels in Barrington's nucleus between reversal groups (p = 0.42) (Fig. B), possibly indicating a direct effect on the bladder rather than a persistent stress effect. There were no differences in the contractility of bladder wall muscle. CsA decreased the nuclear translocation of MEF-2 and NFAT induced by stress (Fig. C,D). CONCLUSION: CsA reverses stress-induced urinary retention, but does not change the stress-induced CRF increase in Barrington's nucleus. Furthermore, bladder smooth muscle contractility is unchanged by CsA; however, there are changes in the levels of the downstream transcription factors MEF-2 and NFAT. We suspect that additional CsA responsive neural changes play a pivotal role in the abnormal voiding phenotype following social stress.

Role of oxidative stress and mitochondria in onset of urinary bladder dysfunction under acute urine retention.

Acute urine retention is a frequent complication in patients with benign hyperplasia of the prostate gland. According to studies made on experimental animals and people, it is accompanied by the deterioration of the bladder blood supply. This study attempts to explore the relationship of intramural blood flow, production of reactive oxygen species, and functional state of the bladder detrusor in modeling of acute urine retention in rats, as well as the impact of mitochondria-targeted antioxidants (which are supposed to alleviate the effects of oxidative stress induced by experimental ischemia) on these parameters. The study showed beneficial effects of mitochondria-targeted antioxidant SkQR1 in preventing damage of the bladder caused by acute urinary retention, which suggests the therapeutic use of this type of compounds for the treatment of ischemic abnormalities of the urinary bladder.

Expression of Hsp27 correlated with rat detrusor contraction after acute urinary retention.

Heat shock protein 27 (Hsp27) can regulate actin cytoskeleton dynamics and contractile protein activation. This study investigates whether Hsp27 expression is related to bladder contractile dysfunction after acute urinary retention (AUR). Female rats were randomized either to AUR by urethral ligation or to normal control group. Bladder and smooth muscle strip contraction at time points from 0 h to 7 days after AUR were estimated by cystometric and organ bath studies. Hsp27 expression in bladder tissue at each time point was detected with immunofluorescence, Western blots, and real-time PCR. Expression of the three phosphorylated forms of Hsp27 was detected by Western blots. Smooth muscle ultrastructure was observed by transmission electron microscopy. Data suggest that maximum detrusor pressure and both carbachol-induced and spontaneous detrusor strip contraction amplitude decreased gradually for the duration from 0 to 6 h, and then increased gradually to near-normal values at 24 h. Treatment of muscle strips with the p38MAK inhibitor, SB203580, inhibited carbachol-induced contractions. Smooth muscle ultrastructure damage was the highest at 6 h after AUR, and then lessened gradually during next 7 days, and ultrastructure was close to normal. Expressions of Hsp27 mRNA and protein and the proteins of the three phosphorylated forms were higher at 0 h, decreased to lower levels up to 6 h, and then gradually increased. Therefore, we conclude that rat bladder contractile function after AUR worsens during 0-6 h, and then gradually recovers. The findings of the current study suggest that Hsp27 modulates bladder smooth muscle contraction after AUR, and that phosphorylation of Hsp27 may be an important pathway modulating actin cytoskeleton dynamics in bladder smooth muscle contraction and reconstruction after injury.

PTHrP is endogenous relaxant for spontaneous smooth muscle contraction in urinary bladder of female rat.

Acute bladder distension causes various morphologic and functional changes, in part through altered gene expression. We aimed to investigate the physiologic role of PTHrP, which is up-regulated in an acute bladder distension model in female rats. In the control Empty group, bladders were kept empty for 6 hours, and in the Distension group, bladders were kept distended for 3 hours after an artificial storing-voiding cycle for 3 hours. In the Distention group bladder, up-regulation of transcripts was noted for 3 genes reported to be up-regulated by stretch in the cultured bladder smooth muscle cells in vitro. Further transcriptome analysis by microarray identified PTHrP as the 22nd highest gene up-regulated in Distension group bladder, among more than 27,000 genes. Localization of PTHrP and its functional receptor, PTH/PTHrP receptor 1 (PTH1R), were analyzed in the untreated rat bladders and cultured bladder cells using real-time RT-PCR and immunoblotting, which revealed that PTH1R and PTHrP were more predominantly expressed in smooth muscle than in urothelium. Exogenous PTHrP peptide (1-34) increased intracellular cAMP level in cultured bladder smooth muscle cells. In organ bath study using bladder strips, the PTHrP peptide caused a marked reduction in the amplitude of spontaneous contraction but caused only modest suppression for carbachol-induced contraction. In in vivo functional study by cystometrogram, the PTHrP peptide decreased voiding pressure and increased bladder compliance. Thus, PTHrP is a potent endogenous relaxant of bladder contraction, and autocrine or paracrine mechanism of the PTHrP-PTH1R axis is a physiologically relevant pathway functioning in the bladder.

[Effects of electroacupuncture of "Weizhong" (BL 40), "Sanyinjiao" (SP 6) and "Yinlingquan" (SP 9) on intravesical pressure and bladder adenosine triphosphate content in rabbits with acute urinary retention].

OBJECTIVE: To observe the effect of electroacupuncture (EA) of "Weizhong" (BL 40), "Sanyinjiao" (SP 6) and "Yinlingquan" (SP 9) on changes of intravesical pressure and contents of adenosine triphosphate (ATP) in the urinary bladder tissue in rabbits with acute urine retention, so as to explore the relatively specificity of acupoints for urinary bladder problems. METHODS: Forty-eight male adult rabbits were randomly divided into normal control, model, Weizhong (BL 40, EA-BL 40), San-yinjiao (SP 6, EA-SP 6), Yinlingquan (SP9, EA-SP9) and non-acupoint (EA-NA) groups. Acute urinary retention model was established by filling the rabbits' bladder with normal saline at a volume of 2 times above their normal capacity for 2 hours. EA (2 Hz/15 Hz, 0.6 mA) was applied to bilateral "Weizhong" (BL 40), "Sanyinjiao" (SP 6) and "Yinlingquan" (SP 9) for 20 min, respectively. Intravesical pressure was detected by using a pressure transducer and an amplifier. Bladder ATP content was detected by using enzyme linked immunosorbent assay (ELISA). RESULTS: In comparison with pre-modeling, the intravesical pressure levels were decreased significantly after modeling in the model, EA-BL 40, EA-SP 6, EA-SP 9 and EA-NA groups (P < 0.05). Compared with pre-EA, intravesical pressure values were increased remarkably in the EA-BL 40, EA-SP 6, EA-SP 9 and EA-NA groups (P < 0.05). The percentages of the increased vesical pressure after EA were considerably higher in the EA-BL 40, EA-SP 6, EA-SP 9 and EA-NA groups than in the model group (P < 0.05). Compared with the normal group, bladder ATP content in the model group was reduced significantly (P < 0.05); while in comparison with the model group, ATP contents in the EA-BL 40, EA-SP 6 and EA-SP 9 groups were up-regulated apparently (P < 0.05). The bladder ATP level of the EA-BL 40 group was significantly higher than those of EA-SP 6 and EA-SP 9 groups (P < 0.05). No significant differences were found between the model and EA-NA groups, and between the EA-SP6 and EA-SP9 groups in bladder ATP contents (P > 0.05), and among the EA-BL 40, EA-SP 6 and EA-SP 9 groups in the percentages of the increased intravesical pressure (P > 0.05). CONCLUSION: EA of BL 40, SP 6 and SP 9 can significantly raise intravesical pressure and bladder ATP content in urine retention rabbits, which may contribute to its effect in improving urinary retention.

SM2(+/-) male mice are predisposed to develop urinary tract obstruction and hyper contractility of the bladder smooth muscle upon ageing.

We previously showed that complete loss of smooth muscle myosin heavy chain isoform 2 (SM2) resulted in postnatal lethality, but in het mice a partial loss of SM2 (SM2(+/-)) was accompanied by down-regulation of SM1 with unaltered SM2:SM1 ratio. To determine whether a normal bladder function would be maintained throughout its lifespan, we aged WT and SM2(+/-) mice up to 18 months and analyzed a) SM2:SM1 ratio b) bladder smooth muscle structure and c) function in SM2(+/-) het mice. A notable finding was that ~50% of 15-18 months old male SM2(+/-) mice exhibited urinary retention in bladder with the distention of upper urethra. In SM2(+/-) mouse bladder with urinary retention, the SM2:SM1 ratio was decreased but not in SM2(+/-) mouse bladder that did not develop urinary retention. Interestingly in the distended bladder the expression levels of α-actin and tropomyosin remained unaltered despite a reduction in the number of myosin thick filaments. These distended bladders showed hypersensitivity to submaximal K(+) depolarization and M3-receptor stimulation, without a significant increase in myosin light chain phosphorylation. We therefore suggest that a partial loss of SM2 may predispose male mice to develop lower urinary tract obstruction during ageing. In addition our data suggest that bladder obstruction can cause a further reduction in SM2 expression and SM2:SM1 ratio, and a hyper-contractility of the bladder smooth muscle.

PARP inhibition prevents oxidative injury of bladder induced by acute urinary retention and subsequent emptying.

It has been demonstrated that increases in poly(ADP-ribose) polymerase (PARP) activity causes damage to several organs under ischemia/reperfusion (I/R) conditions. The aims of this study were to investigate whether inhibition of PARP could suppress apoptosis in the bladder following acute urinary retention (AUR) and subsequent bladder emptying. Twelve-week-old male Sprague Dawley rats were divided into a control group, saline treated group, and 3-aminobenzamide (3-AB, a specific PARP inhibitor)-treated group. Sixty minutes after the administration of saline and 3-AB, the saline and 3-AB-treated groups had 60 min of over-distension and followed by 2 h of drainage. The degree of bladder apoptosis, levels of malondialdehyde (MDA), ATP and nicotinamide adenine dinucleotide (NAD+); expression of poly(ADP-ribose) (PAR), phosphorylation of protein kinase B (Akt); and levels of Bcl-2, Bax, and caspase 3 activity in the bladder were determined. Molecular and histological analyses showed that bladder apoptosis was associated with increases in the amount of PAR and decreases in ATP and NAD+ levels in the saline treated group. In addition, phosphorylated Akt and Bcl-2/Bax ratio were significantly decreased. The activity of caspase 3 was significantly increased in the saline treated group. Inhibition of PARP significantly increased the levels of ATP and NAD+, phosphorylation of Akt, and Bcl-2/Bax ratio, and significantly reduced the activation of caspase 3. As a result, apoptosis in the bladder was attenuated. These results indicate that PARP activation may be involved in apoptosis in the bladder induced by AUR and subsequent emptying via energy depletion and suppression of Akt activity.

Body fluid retention and body weight change in anorexia nervosa patients during refeeding.

BACKGROUND & AIMS: Body weight gain is an important goal in anorexia nervosa (AN) patients, but inflation in body fluids could artificially increase body weight during refeeding. METHODS: 42 malnourished adult AN patients were refed using a normal-sodium diet, then 176 other malnourished adult AN patients received a refeeding low-sodium diet (BMI of the 218 patients: 13.4 ± 1.9 kg/m(2)). Sodium balance, body composition by a 2-electrode impedance method (BIA, for assessment of total and extracellular water, fat-free mass, FFM), resting energy expenditure and energy intake were calculated. RESULTS: In the patients on normal-sodium diet, body weight, and total and extracellular water gains were higher than those of the low-sodium diet patients (P<0.01). Edema occurred more often in the former group (21% vs 6%; P<0.05). In almost all patients, BMI reached a plateau around 15-16 kg/m(2), then increased again. During this plateau, an increase in intracellular water and in "active FFM" was observed with BIA, together with a similar decrease in extracellular water. CONCLUSION: In AN patients, who are always afraid of gaining too much weight, in regard to their food intake, it will be useful to give a low-sodium diet until a 15-16 kg/m(2) BMI. This should be integrated into the cognitive behavioral therapy.

The role of ATP-sensitive potassium channel on acute urinary retention and subsequent catheterization in the rat.

We investigated the role of K(ATP) channel on acute urinary retention (AUR) induced bladder dysfunction. Eight-week-old female Sprague-Dawley rats were divided into seven groups: a sham-operated control group, an AUR group, and five AUR groups treated with: two different K(ATP) channel openers namely nicorandil (3 or 10mg/kg), or cromakalim (100 or 300microg/kg), or one K(ATP) channel inhibitor namely glibenclamide (5mg/kg). The drugs were administered 30min before induction of AUR. After the urethra was obstructed with a clip, AUR was induced by intravesical infusion of 2.5ml of saline via cystostomy. Following a 30min obstruction the bladder was allowed to drain with a catheter in place for 60min with real-time monitoring of intravesical pressure and blood flow. After the experimental period, the bladder function was assessed, using organ bath techniques (carbachol and 100mM KCl). AUR increased the intravesical pressure and decreased the blood flow. The subsequent catheterization decreased the intravesical pressure and increased the blood flow. AUR group reduced significantly the contractile responses to both carbachol and KCl compared with the control group. Nicorandil and cromakalim but not glibenclamide prevented the bladder dysfunction after AUR suggesting that K(ATP) channel openers may prevent the bladder dysfunction caused by AUR and subsequent catheterization.

[Effect of electroacupuncture of different acupoints on the excitability of detrusor muscle and the expression of BDNF and TrkB in the spinal cord of rats with urinary retention due to spinal cord injury].

OBJECTIVE: To observe the effect of electroacupuncture (EA) of different acupoints on the expression of brain-derived neurotrophic factor (BDNF) and tropomyosine receptor kinase B (TrkB) in the spinal cord and the excitability of detrusor muscle of the uninary bladder in rats with urinary retention owing to spinal cord injury (SCI). METHODS: A total of 100 female SD rats were randomly divided into normal, sham-operation (sham), model, EA-Guanyuan (CV 4), and EA-Shuidao (ST 28) groups, with 20 cases in each. SCI induced urinary retention model was established by using weight dropping method. EA (1 mA, 2 Hz/15 Hz) was applied to "Guanyuan" (CV 4) and "Shuidao" (ST 28) respectively for 20 min, once a day for 10 days. The excitability (tone, contraction frequency) of the detrusor muscle of the bladder was detected in vitro by using electrophysiological method, and the expression of BDNF and TrkB in spinal cord was determined by immunohistochemistry staining. RESULTS: In comparison with normal control and sham groups, the tension and the contraction frequency of detrusor muscle in model group lowered significantly (P<0.05), while compared with model group, both the tension and contraction frequency of detrusor muscle increased pronouncedly in EA-CV 4 and EA-ST 28 groups (P<0.05), and the effect of EA-CV 4 was apparently superior to that of EA-ST 28 (P<0.05). In comparison with normal and sham groups, the BDNF and TrkB immunoreaction positive cells in the spinal cord were significantly more in model group (P<0.05). Compared with model group, those of EA-CV 4 and EA-ST 28 groups were obviously further increased (P<0.05), and the effect of EA-CV 4 group was markedly superior to that of EA-ST 28 group (P<0.05). CONCLUSION: EA of CV 4 and ST 28 can raise the excitability of the smooth muscle of the uninary bladder in rats with SCI-induced urinary retention, which may be related to its effects in upregulating the expression of BDNF and TrkB in the spinal cord. The effects of EA of CV 4 were evidently superior to those of EA of ST 28.

Sodium retention and ascites formation in a cholestatic mice model: role of aldosterone and mineralocorticoid receptor?

UNLABELLED: Renal sodium retention in experimental liver cirrhosis originates from the distal nephron sensitive to aldosterone. The aims of this study were to (1) determine the exact site of sodium retention along the aldosterone-sensitive distal nephron, and (2) to evaluate the role of aldosterone and mineralocorticoid receptor activation in this process. Liver cirrhosis was induced by bile duct ligation in either adrenal-intact or corticosteroid-clamped mice. Corticosteroid-clamp was achieved through adrenalectomy and corticosteroid supplementation with aldosterone and dexamethasone via osmotic minipumps. 24-hours renal sodium balance was evaluated in metabolic cages. Activity and expression of sodium- and potassium-dependent adenosine triphosphatase were determined in microdissected segments of nephron. Within 4-5 weeks, cirrhosis induced sodium retention in adrenal-intact mice and formation of ascites in 50% of mice. At that time, sodium- and potassium-dependent adenosine triphosphatase activity increased specifically in cortical collecting ducts. Hyperaldosteronemia was indicated by increases in urinary aldosterone excretion and in sgk1 (serum- and glucocorticoid-regulated kinase 1) mRNA expression in collecting ducts. Corticosteroid-clamp prevented induction of sgk1 but not cirrhosis-induced sodium retention, formation of ascites and stimulation of sodium- and potassium-dependent adenosine triphosphatase activity and expression (mRNA and protein) in collecting duct. These findings demonstrate that sodium retention in cirrhosis is independent of hyperaldosteronemia and of the activation of mineralocorticoid receptor. CONCLUSION: Bile duct ligation in mice induces cirrhosis which, within 4-5 weeks, leads to the induction of sodium- and potassium-dependent adenosine triphosphatase in cortical collecting ducts, to renal sodium retention and to the formation of ascites. Sodium retention, ascites formation and induction of sodium- and potassium-dependent adenosine triphosphatase are independent of the activation of mineralocorticoid receptors by either aldosterone or glucocorticoids.

Does two episodes of acute urinary retention lead to additional ischemia-reperfusion injury in rat bladder?

AIM: To determine whether two episodes of acute urinary retention lead to additional ischemia-reperfusion injury due to decompression of the bladder, or not. MATERIALS AND METHODS: Sham, retention and recurrent retention groups consisting of 5, 8 and 8 Wistar Albino male rats were randomized, respectively. After the bladders of rats were emptied with 3F catheter, penile urethras were clamped with aneurism clamp and waited for 30 min after diuresis was forced. At the end of this period, penile clamps were removed and the bladder was again decompressed with 3F catheter and after 30 min removed for examination. In the recurrent retention group, the same process was repeated after an interval of one week. Malonedialdehyde (MDA) levels, indicator of lipid peroxidation and myeloperoxidase (MPO) levels, indicator of leukocyte activation, were examined biochemically in the tissues of the removed bladders. RESULTS: In the retention and recurrent retention groups, the average increase in bladder MDA and MPO values was higher than the values of sham group (P < 0.05), however, no significant difference was determined between retention and recurrent retention groups (P > 0.05). CONCLUSION: In the bladder tissue, due to acute urinary retention and following decompression process, ischemia-reperfusion injury occurs. Two episodes of acute urinary retention do not lead to additional the ischemia-reperfusion injury that develops in the bladder.

Sympathetic vesicovascular reflex induced by acute urinary retention evokes proinflammatory and proapoptotic injury in rat liver.

Increased hepatic sympathetic activity affects hepatic metabolism and hemodynamics and subsequently causes acute hepatic injury. We examined whether the vesicovascular reflex evoked by bladder overdistension could affect hepatic function, specifically reactive oxygen species (ROS)-induced inflammation and apoptosis, through activation of the hepatic sympathetic nerve. We evaluated the hepatic hemodynamics, hepatic sympathetic nervous activities, and cystometrograms in anesthetized rats subjected to acute urinary retention. We used a chemiluminescence method, an in situ nitro blue tetrazolium perfusion technique, and a DNA fragmentation/apoptosis-related protein assay to demonstrate de novo and colocalize superoxide production and apoptosis formation in rat liver. Acute urinary retention increased the hepatic sympathetic-dependent vesicovascular reflex, which caused hepatic vasoconstriction/hypoxia and increased superoxide anion production from the periportal Kupffer cells and hepatocytes, which were aggravated by the increase in volume and duration of urinary retention. The ROS-enhanced proinflammatory NF-kappaB, activator protein-1, and ICAM-1 expression also promoted proapoptotic mechanisms, including increases in the Bax/Bcl-2 ratio, CPP32 expression, poly-(ADP-ribose)-polymerase cleavages, and DNA fragmentation and apoptotic cells in the liver. The proinflammatory and proapoptotic mechanisms were significantly attenuated in rats treated with hepatic sympathetic nerve denervation or catechin (antioxidant) supplement. In conclusion, our results suggest that acute urine retention enhances hepatic sympathetic activity, which causes hepatic vasoconstriction and evokes proinflammatory and proapoptotic oxidative injury in the rat liver. Reduction of the hepatic sympathetic tone or antioxidant supplement significantly attenuates these injuries.