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首页> 外文期刊>Drug and Chemical Toxicology >The fibrosis of ketamine, a noncompetitive N-methyl-d-aspartic acid receptor antagonist dose-dependent change in a ketamine-induced cystitis rat model
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The fibrosis of ketamine, a noncompetitive N-methyl-d-aspartic acid receptor antagonist dose-dependent change in a ketamine-induced cystitis rat model

机译：氯胺酮的纤维化，一种非竞争性的N-甲基-d-天冬氨酸受体拮抗剂在氯胺酮诱导的膀胱炎大鼠模型中的剂量依赖性变化

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Ketamine abusers have greatly increased in number worldwide during recent years. The consumption of ketamine has increased, as have the number of published accounts of devastating urological sequelae. However, the mechanism of ketamine-associated urinary tract dysfunction remains unclear. This study was to evaluate the ketamine dose-dependency of ketamine-induced cystitis (KC) in a rat model. A total of 42 Sprague-Dawley rats (female, 10-week-old) were used. Each of the 7 KC rat models were induced by 1, 5, 10, 25 and 50 mg/kg ketamine intravenous injection for two weeks. For the sham group (n = 7), a phosphate-buffered saline (PBS) vehicle was used rather than ketamine hydrochloride. The cystometric parameters, histological examinations, staining for Masson's trichome, cytokeratin, toluidine blue and quantitative PCR were measured at two weeks following the intervention. The voiding interval gradually decreased depending upon the ketamine dose of 1, 5, 10, 25, or 50 mg/kg, respectively, and was decreased compared with Sham. Bladder capacity was decreased as ketamine dose increased. In particular, the increase of fibrosis and submucosal apoptosis were found according to the increase of the ketamine dose. The bladder apoptosis in the KC rat model makes the fibrotic bladder change, and led us to hypothesize that fibrosis could contribute to the lower urinary-tract symptoms. We suggest that according to the pathophysiology evidence, fibrosis induced by apoptosis plays a key role in KC.
机译：近年来，氯胺酮滥用者的数量在全球范围内大大增加。氯胺酮的消费量增加了，破坏性泌尿后遗症的已发表报道数量也有所增加。然而，氯胺酮相关的尿路功能障碍的机制仍不清楚。这项研究旨在评估大鼠模型中氯胺酮诱导的膀胱炎（KC）的氯胺酮剂量依赖性。总共使用42只Sprague-Dawley大鼠（雌性，10周龄）。分别通过1、5、10、25和50 mg / kg氯胺酮静脉内注射诱导7只KC大鼠模型，持续两周。对于假手术组（n = 7），使用磷酸盐缓冲盐水（PBS）介质代替盐酸氯胺酮。干预后两周测量膀胱测量参数，组织学检查，Masson毛状体的染色，细胞角蛋白，甲苯胺蓝和定量PCR。与氯胺酮的剂量分别为1、5、10、25或50 mg / kg相比，排尿间隔逐渐减少，与Sham相比有所减少。随着氯胺酮剂量的增加，膀胱容量降低。特别地，根据氯胺酮剂量的增加，发现纤维化和粘膜下细胞凋亡的增加。 KC大鼠模型中的膀胱凋亡使膀胱纤维化发生改变，并导致我们假设纤维化可导致下尿路症状。我们建议根据病理生理学证据，凋亡诱导的纤维化在KC中起关键作用。

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