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目的探讨氯胺酮性膀胱炎大鼠模型的建立方法,为研究氯胺酮性膀胱炎提供可靠的动物模型。方法将30只雌性SD大鼠随机分为两组,对照组10只,氯胺酮组20只。模型组予氯胺酮30 mg·kg~(-1)腹腔注射,每日1次,共12周。对照组注射等容量生理盐水。检测两组大鼠排尿间隔时间、最大膀胱容量(MBC)、最大排尿压(MVP)和逼尿肌不稳定收缩频率,并比较膀胱病理学差异。结果与给药前比较,给药后氯胺酮组大鼠排尿闾隔时间、MBC随时间进行性下降(P<0.05),逼尿肌不稳定收缩频率进行性增高(P<0.05),MVP无明显变化(P>0.05)。12周后,对照组大鼠排尿间隔时间和MBC均高于氯胺酮组(P<0.01),未测得逼尿肌不稳定收缩频率。与对照组比较,氯胺酮组大鼠膀胱黏膜上皮显著增厚,黏膜下层腺管增粗,腺腔增多、增大,有炎症细胞侵润。结论腹腔注射氯胺酮可以诱导大鼠患氯胺酮性膀胱炎,并可作为研究氯胺酮性膀胱炎的可靠模型。
Objective To investigate the establishment of a rat model of ketamine cystitis and provide a reliable animal model for the study of ketamine cystitis. Methods Thirty female SD rats were randomly divided into two groups: control group (n = 10) and ketamine group (n = 20). The model group was given ketamine 30 mg · kg -1 intraperitoneally once a day for 12 weeks. The control group was injected with normal saline. The urinary interval time, maximum bladder volume (MBC), maximum voiding pressure (MVP) and unstable detrusor contractility frequency were detected in two groups of rats, and bladder pathology was compared. Results Compared with those before administration, the urinary concentration of MBC decreased gradually (P <0.05) and the instability frequency of detrusor instability increased (P <0.05), while the MVP had no significant difference Change (P> 0.05). After 12 weeks, urinary interval time and MBC in control group were significantly higher than those in ketamine group (P <0.01). Unstable instability frequency of detrusor was not detected. Compared with the control group, the ketamine group of rat bladder mucosal epithelium was significantly thicker, submucosal thickening of the duct, glandular cavity increased, increased, infiltration of inflammatory cells. Conclusion Intraperitoneal injection of ketamine can induce ketamine cystitis in rats and can be used as a reliable model for the study of ketamine cystitis.