Abstract
This study aimed to determine the mechanism of ketamine-induced cystitis without metabolism. A total of 24 adult male Sprague-Dawley rats were separated into control, ketamine, and norketamine groups. To induce cystitis, rats in the ketamine and norketamine groups were treated with intravesical instillation of ketamine and norketamine by mini-osmotic pump, which was placed in subcutaneous space, daily for 24 h for 4 weeks. After 4 weeks, all rats were subjected to bladder functional tests. The bladders were collected for histological and pathological evaluation. Compared to control, ketamine treatment demonstrated an increase in the bladder weight, high bladder/body coefficient, contractive pressure, voiding volume, collagen deposition, reduced smooth muscle content, damaged glycosaminoglycan layer, and low bladder compliance. Compared to ketamine, norketamine treatment showed more severe collagen deposition, smooth muscle loss, damaged glycosaminoglycan layer, and increased residual urine. Intravesical administration of ketamine and norketamine induced cystitis with different urodynamic characteristics. Norketamine treatment caused more severe bladder dysfunction than ketamine treatment. Direct treatment of the bladder with norketamine induced symptoms more consistent with those of bladder outlet obstruction than ketamine cystitis. Detailed studies of cellular mechanisms are required to determine the pathogenesis of ketamine cystitis.
Highlights
Ketamine is a derivative of phencyclidine (PCP) and absorbed in humans
Rats in the ketamine group were treated with the intravesical instillation of ketamine hydrochloride (100 mg/mL) 24 h daily for 4 weeks; the norketamine group was treated with the intravesical instillation of norketamine hydrochloride (10 mg/mL) for 24 h daily for
The study demonstrated that the intravesical administration of ketamine and norketamine induced cystitis with different urodynamic characteristics and pathological changes
Summary
Ketamine is a derivative of phencyclidine (PCP) and absorbed in humans. It is characterized as an N-methyl-D-aspartic acid receptor (NMDAR) antagonist and is a useful analgesic and anesthetic discovered in 1956 and approved by the FDA in 1970 for the use in humans as an anesthetic [1,2,3,4,5]. Because the pathogenesis of ketamine-induced cystitis is still unclear, medical treatment is based on resolving or reducing the symptoms of pain or inflammation, including oral medication, hyperbaric-oxygen therapy, cystoscopic hydrodistention, intravesical medicine injection, or instillation (such as hyaluronic acid, anticholinergic agents, non-steroid or steroid antiinflammatory drugs, and botulinum toxin A) [11,12,15,16,17,18]. To cure ketamine-induced cystitis, determining the pathophysiology and etiology of the disease is important
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