An optimized transurethral catheterization cystometry in mice and comparison with classic suprapubic catheterization cystometry

Section: Discussionmentioning

confidence: 99%

“…A slow saline infusion rate (0.6 mL/h) may produce misleading estimations. Due to the long period (at least 1 h) required for cystometry investigations, the real BC should include the volume of saline infused to induce the voiding and a high proportion of self‐produced urine.…”

Section: Discussionmentioning

confidence: 99%

Suture causing urethral meatus stricture: A novel animal model of partial bladder outlet obstruction

Chen

Yang

et al. 2018

“…Pentobarbital sodium in dose of 6 mg/kg was intraperitoneally injected to anesthetize mice. A standardized surgery procedure was used to create pBOO as described in our previous study . Briefly, after transurethrally inserting a PE10 tube, a lower midline incision (5 mm) was made to allow separating the urethra free from surrounding tissues.…”

Section: Methodsmentioning

confidence: 99%

“…TUCC was performed as previously described to evaluate the mice bladder function. Urethane (1.2 mg/kg, i.p) was used to anaesthetize mice.…”

Section: Methodsmentioning

confidence: 99%

“…A standardized surgery procedure was used to create pBOO as described in our previous study. 19 Briefly, after transurethrally inserting a PE10 tube, a lower midline incision (5 mm) was made to allow separating the urethra free from surrounding tissues. A 4-0 nylon ligature was tied around the urethra, then the PE10 tube was removed before incision closed.…”

Section: Animals and Partial Bladder Outlet Obstruction Surgerymentioning

confidence: 99%

See 1 more Smart Citation

Responses of bladder smooth muscle to the stretch go through extracellular signal‐regulated kinase (ERK)/p90 ribosomal S6 protein kinase (p90RSK)/Nuclear factor‐κB (NF‐κB) Pathway

Lin

et al. 2019

Self Cite

Aims The present study was designed to study changes and its potential mechanisms in human bladder smooth muscle subjected to stretch. Methods Bioinformatics analyses including differential expression analysis, overrepresentation enrichment analysis, principal component analysis, and weighted gene coexpression network analysis were used to analyze a microarray dataset (GSE47080) of partial bladder outlet obstruction (pBOO) in rat to find the potential changes of gene expressions. Bladder from pBOO model and human bladder smooth muscle cells (HBSMCs) subjected to sustained prolonged stretch were collected for Western blot analysis, real‐time polymerase chain reaction, and fluorescence analysis to verify the changes of gene expressions and preliminarily study the potential role of signaling pathway regulation in treatment of pBOO. Results The bioinformatics analysis showed that chronic obstruction activated mitogen‐activated protein kinase pathway and changed cytoskeleton structure in bladder smooth muscle. In in vivo experiments in mice, pBOO was verified by cystometry. Partial BOO activated the extracellular signal‐regulated kinase (ERK)/p90 ribosomal S6 protein kinase (p90RSK)/nuclear factor‐κB (NF‐κB) signaling pathway in DM. The messenger RNA (mRNA) expressions of contractile phenotypic proteins increased after pBOO. In in vitro experiments of HBSMCs, mechanical stretch activated ERK/p90RSK/NF‐κB in HBSMCs in a time‐dependent manner. The mRNA expressions of α‐smooth muscle actin and SM22 also increased and filamentous actin (F‐actin) polymerization was enhanced as well. Inhibition of ERK/p90RSK/NF‐κB pathway reversed mechanical stretch‐induced changes of contractile phenotypic expression and F‐action polymerization. Conclusions Continuous stretch increases expressions of contractile phenotypic proteins and promotes the polymerization of F‐actin. This process partially goes through ERK/p90RSK/NF‐κB pathway.

The intracerebroventricular injection of lipopolysaccharide may induce neurogenic detrusor overactivity symptoms in mice

Chen

Yang

Tong

et al. 2022

Purpose We aimed to explore if the intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS) was able to evoke the cognitive and locomotive impairment and detrusor overactivity (DO) symptoms in mice. Methods This study compared the bladder function of mice that received the i.c.v. injection of LPS or saline. Specifically, basal pressure (BP), threshold pressure (TP), micturition pressure (MP), bladder capacity (BC), micturition volume (MV), bladder compliance (COM), frequency of micturition (MF), detrusor overactive index (DOI), frequency of non‐voiding contractions (FNVCs), and amplitude of non‐voiding contractions (ANVCs) were assessed by cystometry. The spontaneous voiding spot assay (VSA) was exerted to further assess the micturition patterns of mice. The Morris water maze (MWM) and the open field test (OFT) were used to detect the cognition and locomotive behaviors, respectively. Hematoxylin and eosin staining was conducted to evaluate the changes in morphology and histology of mice. The extent of injury in the prefrontal cortex was tested by using Nissl staining. Results The LPS‐treated mice exhibited evidently DO characterized by the increase of MF, FNVCs, ANVCs, and DOI and the decrease of BC. The VSA further suggested that LPS induced urinary frequency and urinary incontinence in mice. Furthermore, neither signs of bladder inflammation nor the damage of bladder smooth muscle and urothelium in LPS‐exposed mice was observed. LPS induced deficits in spatial learning, memory, and locomotor activity in mice. Neuronal cells in the prefrontal cortex were obviously lost in the LPS‐treated mice. Conclusions Acute neuroinflammation induced the cognitive and locomotive impairment and the neurogenic overactive bladder (NOAB) symptoms in mice. This novel animal model may contribute to further study the mechanisms of NOAB in neurodegenerative patients and assess the novel therapeutic strategies in the future.