AimsTo determine whether ultrasound‐assisted prompted voiding (USAPV) care is more efficacious than conventional prompted voiding (CPV) care for managing urinary incontinence in nursing homes.MethodsThirteen participating nursing homes in Japan were randomized to CPV (n = 7) or USAPV care group (n = 6). Residents of the allocated nursing homes received CPV (n = 35) or USAPV (n = 45) care for 8 weeks. In the CPV group, caregivers asked the elderly every 2‐3 h whether they had a desire to void and prompted them to void when the response was yes. In the USAPV group, caregivers regularly monitored bladder urine volume by an ultrasound device and prompted them to void when the volume reached close to the individually optimized bladder capacity. Frequency‐volume chart was recorded at the baseline and after the 8‐week intervention to measure the daytime urine loss.ResultsThe change in daytime urine loss was statistically greater in the USAPV (median, −80.0 g) than in the CPV (median, −9.0 g; P = .018) group. The proportion of elderly individuals whose daytime urine loss decreased by >25% was 51% and 26% in the USAPV and CPV group, respectively (P = .020). Quality‐of‐life measures of elderly participants showed no significant changes in both groups. The care burden scale score of caregivers was unchanged in the USAPV group (P = .59) but significantly worsened in the CPV group (P = .010) after the intervention.ConclusionsUSAPV is efficacious and feasible for managing urinary incontinence in nursing homes.
We investigated age-related changes in in vivo and in vitro functions and gene expression of the bladder of male and female mice. Mature and aged (12 and 27–30 month old) C57BL/6 mice of both sexes were used. Frequency volume, conscious free-moving cystometry and detrusor contractile and relaxant properties in in vitro organ bath were evaluated. mRNA expression level of muscarinic, purinergic, and β-adrenergic receptors and gene expression changes by cDNA microarray analysis of the bladder were determined. Cystometry demonstrated storage and voiding dysfunctions with ageing in both sexes. Detrusor strips from aged mice showed weaker contractile responses particularly in the cholinergic component and weaker relaxant responses to isoproterenol. These age-related impairments were generally severer in males. mRNA expression of bladder tissue was decreased for M3 muscarinic receptors in aged males and β2-adrenoceptors in aged females. cDNA microarray analysis results, albeit substantial sex difference, indicated “cell-to-cell signaling and interaction” as the most common feature of age-related gene expression. In summary, aged mice demonstrated voiding and storage dysfunctions resembling to detrusor hyperactivity with impaired contractility (DHIC), which were more pronounced in males. Genomic changes associated with aging may contribute to the age-related bladder functional deterioration in mice.
Toll-like receptor 7 (TLR7) is associated with the pathophysiology of systemic lupus erythematosus and Sjögren syndrome, well-known diseases accompanying interstitial cystitis (IC). We studied TLR7 expression in the bladder of patients with Hunner-type IC (HIC) and its functional roles in bladder inflammation and nociception using mice. Bladder biopsy specimens were obtained from patients with HIC. Specimens from the noncancerous portion of the bladder of patients with bladder cancer served as controls. The specimens were examined by immunohistochemistry and real-time polymerase chain reaction of TLR7. Loxoribine (LX), a TLR7 agonist, was instilled in the bladder of C57BL/6N female mice, and TLR7-mRNA expression and histological changes of the bladder, bladder pain-like licking behavior, voiding behavior, cystometry, and bladder afferent nerve activities were investigated. The effects of hydroxychloroquine, a TLR7 antagonist, on the LX-induced changes on cystometry and voiding behavior were studied. The number of TLR7 immuno-reactive cells and the mRNA expression of TLR7 were significantly increased in HIC specimens. Intravesical instillation of LX induced edema, congestion, inflammation, and significantly increased TLR7-mRNA expression in the mouse bladder. Loxoribine-instillation also significantly increased licking behavior, voiding frequency, and afferent nerve activities associated with decreased single-voided volume and intercontraction interval of micturitions. Hydroxychloroquine reversed the LX-induced cystometric and voiding behavioral changes. Toll-like receptor 7 was up-regulated in the bladder mucosa of patients with HIC, and activation of TLR7 in the mouse bladder induced cystitis with sensory hyperactivity of the bladder. Blocking the TLR7 pathway may be an innovative treatment target of HIC.
Transient receptor potential ankyrin 1 (TRPA1) channel expressed by urothelial cells and bladder sensory nerve fibers might act as a bladder mechanosensor and nociceptive transducer. To disclose the role of TRPA1 in bladder function and inflammation-associated hypersensitivity, we evaluated in vitro and in vivo bladder function and inflammatory mechanosensory and nociceptive responses to intravesical lipopolysaccharide (LPS)-instillation in wild type (WT) and TRPA1-knock out (KO) mice. At baseline before treatment, no significant differences were observed in frequency volume variables, in vitro detrusor contractility, and cystometric parameters between the two groups in either sex. LPS-instillation significantly increased voiding frequency and decreased mean voided volume at 24–48 hours after instillation in WT but not in TRPA1-KO mice. LPS-instillation also significantly increased the number of pain-like behavior at 24 hours after instillation in WT mice, but not in TRPA1-KO mice. Cystometry 24 hours after LPS-instillation revealed shorter inter-contraction intervals in the WT mice compared with TRPA1-KO mice. In contrast, inflammatory cell infiltration in the bladder suburothelial layer was not significantly different between the two groups. These results indicate that TRPA1 channels are involved in bladder mechanosensory and nociceptive hypersensitivity accompanied with inflammation but not in physiological bladder function or development of bladder inflammation.
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