Rodent models of ketamine‐induced cystitis

Sultana, Saki; Berger, Geraint; Cox, Ashley; Kelly, Melanie E. M.; Lehmann, Christian

doi:10.1002/nau.24763

Cited by 8 publications

(4 citation statements)

References 53 publications

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“…However, sustained exposure to ketamine might induce persistent inflammations mediated by neurogenic, IgE, or NOS-COX, tailed by collagen accumulation and fibrosis in the urinary bladder, which leads to the thickened bladder wall conditions [7]. Additionally, muscle hypertrophy, submucosal fibrosis, and alterations in the collagen muscle ratio are further common pathological attributes noted in KC patient bladders [14], which were found in the present study observations at different time courses.…”

Section: Discussionsupporting

confidence: 58%

Specific Impacts of Ketamine on Bladder Dysfunction and Associated Histological Alterations in Rats—A Time Course Validation through Transmission Electron Microscopy

Chung

Rajneesh

Chen

et al. 2022

IJMS

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This study explored the specific effects of ketamine on bladder function followed by a sequence of histological changes in a rat bladder at fixed time course intervals. The rats were grouped into normal control and experimental animals, and ketamine (100 mg/kg/day) was administrated to the experimental animals for 2, 4, and 8 weeks, respectively; similarly, the control animals received saline. All animals were evaluated for bladder function and histological responses to the treatment. Ultrastructural changes were observed by transmission electron microscopy (TEM). The results showed progressive bladder dysfunctions with hyperactive bladder conditions according to the time course and frequency of exposure to ketamine. Significantly, decreased inter contraction intervals, residual urine volume, peak micturition pressure, and increased micturition frequency were observed. Bladder histology results revealed substantial inflammation and comprehensive submucosa edema in week 2 and 4 rats along with fibrosis and significant bladder detrusor hypertrophy in week 8 rats. TEM analysis revealed bladder wall thickening, deformed blood vessels, detrusor hypertrophy, wobbled gap junction, and barrier dysfunction at different time course levels in experimental animals. These results provided a profound knowledge about the prognosis and step-by-step pathophysiology of the disease, which might help in developing new therapeutic interventions.

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Section: Discussionsupporting

confidence: 58%

Specific Impacts of Ketamine on Bladder Dysfunction and Associated Histological Alterations in Rats—A Time Course Validation through Transmission Electron Microscopy

Chung

Rajneesh

Chen

et al. 2022

IJMS

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“…However, there remains considerable variation in rodent models in terms of animal strain, dose and duration of ketamine administration and study outcomes. A recent review by Sultana et al 29 provides a summary of current rodent models of KIC but notes that the lack of a standardized KIC model makes it difficult to translate findings to clinical models. Therefore, creating an animal model of KIC and that is consistent across research groups is essential to effectively study KIC pathophysiology and to translate treatments into human studies.…”

Section: Treatment Of Ketamine Induced Cystitis In Animal Modelsmentioning

confidence: 99%

Current approaches for the treatment of ketamine‐induced cystitis

Zhou

Scott

Miab

et al. 2023

Neurourology and Urodynamics

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Aims Ketamine is a dissociative anesthetic, historically used in a clinical setting for the induction and maintenance of anesthesia. Ketamine usage can produce undesirable psychological manifestations including hallucinations and long‐term psychotomimetic effects. As a results of its fast onset and short period of action, ketamine is widely used as a recreational drug. Chronic abuse of ketamine can lead to significant urinary system complications including ketamine‐induced cystitis (KIC). Common side effects of chronic ketamine abuse are urinary pain and discomfort and decreased bladder compliance and voiding pressure. Cessation of ketamine use is associated with improvement of symptoms however the exact pathophysiology of KIC remains unknown, complicating the ability of clinicians to treat this condition. Method A literature search was performed using the National Center for Biotechnology Information (NCBI) Pubmed database up to May 2021. Results Animal models of KIC are necessary to further our understanding of KIC pathophysiology and explore potential treatment options. In all cases, cessation of ketamine use is the first line of treatment and is most effective in managing KIC. In addition to cessation, treatment plans must be tailored to the individual, based on the severity of symptoms and disease progression, and include options such as: oral anti‐inflammatories, intravesical treatment and in the most severe cases, surgical intervention. Conclusion KIC is a painful condition that currently lacks standardized treatment methods. Both animal models of KIC and clinical trials to further elucidate the mechanism of KIC pathophysiology must be explored to create targeted treatment plans.

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“…The first case of ketamine-induced cystitis was described as an abuser in 2007, and approximately 30% of ketamine abusers have been reported to suffer from urinary problems. The severity of ketamine-associated lower urinary tract symptoms is significantly related to both the duration and the dosage of ketamine [1,35]. Urological side effects of ketamine can develop when 2 g or more of ketamine is administered at least three times a week for 1 year.…”

Section: Ketaminementioning

confidence: 99%

Drug-Related Cystitis: An Overview

Engin

2023

Cystitis - Updates and Challenges

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Cystitis is an inflammatory condition of the urinary bladder with infectious or noninfectious aetiologies. Chemical-induced cystitis represents a relatively highly prevalent kind of noninfectious cystitis resulting from therapeutic agents or environmental chemicals. Drug-related cystitis is a type of urotoxicity of drugs, which is a commonly underreported condition leading to impaired quality of patients’ life, discontinuation of medication and non-compliance. Drug-related cystitis can occur in several forms ranging from mild urinary symptoms to gross haematuria, which can be challenging for physicians to treat. Chemotherapeutic drugs, ketamine, tiaprofenic acid and several drugs have been reported to be associated with cystitis until now. Cyclophosphamide (CP) is an alkylating agent that leads to haemorrhagic cystitis with widespread awareness due to its high prevalence in patients under treatment intravenously. However, several currently available drugs have been also reported to induce cystitis, which may be usually ignored. Drug-related cystitis can cause emergency admissions and prolonged hospitalisation, leading to increased medical costs. Some cases of drug-related cystitis are clinically managed with established therapeutic interventions and/or prophylaxis, such as CP-induced haemorrhagic cystitis. On the other hand, standard treatment is currently unavailable for most cases. This chapter will provide current knowledge regarding the drug-related cystitis that should be taken into consideration as a potential adverse effect of drugs by physicians.

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Rodent models of ketamine‐induced cystitis

Cited by 8 publications

References 53 publications

Specific Impacts of Ketamine on Bladder Dysfunction and Associated Histological Alterations in Rats—A Time Course Validation through Transmission Electron Microscopy

Specific Impacts of Ketamine on Bladder Dysfunction and Associated Histological Alterations in Rats—A Time Course Validation through Transmission Electron Microscopy

Current approaches for the treatment of ketamine‐induced cystitis

Drug-Related Cystitis: An Overview

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