Evidence map›Paper›PMID 26911853›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Intact urothelial barrier function in a mouse model of ketamine-induced voiding dysfunction.

Retnagowri Rajandram, Teng Aik Ong, Azad H A Razack, Bryce MacIver, Mark Zeidel, Weiqun Yu

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Dysregulation of CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Causes Urinary Bladder Dysfunction with Abnormal Smooth Muscle Contractility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  6. Real-Time Void Spot Assay.Journal of visualized experiments : JoVE · 2023
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  12. Review
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  17. Molecular mechanisms of voiding dysfunction in a novel mouse model of acute urinary retention.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Retnagowri RajandramDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachuesetts; Department of Surgery, Faculty of Medicine, Kuala Lumpur, Malaysia; and.
Teng Aik OngDepartment of Surgery, Faculty of Medicine, Kuala Lumpur, Malaysia; and University Malaya Medical Centre, Kuala Lumpur, Malaysia.
Azad H A RazackDepartment of Surgery, Faculty of Medicine, Kuala Lumpur, Malaysia; and University Malaya Medical Centre, Kuala Lumpur, Malaysia.
Bryce MacIverDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachuesetts;
Mark ZeidelDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachuesetts;
Weiqun YuDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachuesetts; wyu2@bidmc.harvard.edu.
University Malaya Medical Centre · MYHospital Kuala Lumpur · MY

Funding

Purinergic Regulation of Bladder Interstitial Cells of CajalR00DK095922 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI YU, WEIQUN · 2015 to 2017
$747k
NIDDK NIH HHS R00 DK095922
6 · The paper itself

Abstract

Ketamine is a popular choice for young drug abusers. Ketamine abuse causes lower urinary tract symptoms, with the underlying pathophysiology poorly understood. Disruption of urothelial barrier function has been hypothesized to be a major mechanism for ketamine cystitis, yet the direct evidence of impaired urothelial barrier function is still lacking. To address this question, 8-wk-old female C57BL/6J mice were injected intraperitoneally with 30 mg·kg(-1)·day(-1) ketamine for 12 wk to induce ketamine cystitis. A spontaneous voiding spot assay showed that ketamine-treated mice had increased primary voiding spot numbers and smaller primary voiding spot sizes than control mice (P < 0.05), indicating a contracted bladder and bladder overactivity. Consistently, significantly increased voiding frequency was observed in ketamine-treated mice on cystometrograms. These functional experiments indicate that ketamine induces voiding dysfunction in mice. Surprisingly, urothelial permeability in ketamine-treated mice was not changed when measured using an Ussing chamber system with isotopic urea and water. Mouse urothelial structure was also not altered, and intact umbrella cell structure was observed by both transmission and scanning electron microscopy. Furthermore, immunostaining and confocal microscopy confirmed the presence of a well-defined distribution of zonula occuldens-1 in tight junctions and uroplakin in umbrella cells. In conclusion, these data indicate that ketamine injection induces voiding dysfunction in mice but does not necessarily disrupt mouse bladder barrier function. Disruption of urothelial barrier function may not be the major mechanism in ketamine cystitis.

Indexed as

Anesthetics, DissociativeAnimalsCystitisFemaleKetamineMiceMice, Inbred C57BLPermeabilityTight Junction ProteinsUrinary BladderUrinary Bladder, OveractiveUrotheliumZonula Occludens-1 ProteinAnesthetics, DissociativeKetamineTight Junction ProteinsZonula Occludens-1 Proteinketamine cystitispermeabilityumbrella cellurinary bladdervoiding spot assay

Identifiers

PMID26911853
PMCPMC4867311
OpenAlexW2288256636

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.