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感觉神经元特异性受体激动剂对环磷酰胺诱导的大鼠膀胱炎模型膀胱功能的影响。

Effects of sensory neuron-specific receptor agonist on bladder function in a rat model of cystitis induced by cyclophosphamide.

作者信息

Honda Masashi, Yoshimura Naoki, Kawamoto Bunya, Kobayashi Naoto, Hikita Katsuya, Muraoka Kuniyasu, Saito Motoaki, Sejima Takehiro, Chancellor Michael B, Takenaka Atsushi

机构信息

Department of Urology, Tottori University Faculty of Medicine, 36-1 Nishi, Yonago, 683-8504, Japan.

出版信息

Int Urol Nephrol. 2014 Oct;46(10):1953-9. doi: 10.1007/s11255-014-0734-x. Epub 2014 May 14.

Abstract

PURPOSE

To investigate the effects of activation of sensory neuron-specific receptors (SNSRs) on cyclophosphamide (CYP) bladder overactivity in rats.

METHODS

Female Sprague-Dawley rats (235-258 g) were used. Rats were injected with either CYP (200 mg/kg, intraperitoneally) or saline (control). Continuous cystometrograms (0.04 ml/min) were recorded 48 h after CYP or saline injection under urethane anesthesia. After stable micturition cycles were established, a selective rat SNSR1 agonist, bovine adrenal medulla 8-22 (BAM8-22), was administered intravenously or intrathecally.

RESULTS

Cyclophosphamide treatment-induced higher baseline pressure and shorter intercontraction intervals compared with the control group. Intravenous administration of BAM8-22 at 10, 30 and 100 μg/kg significantly increased intercontraction intervals in the CYP-treated group. Intrathecal administration of BAM8-22 at 0.03, 0.1 and 0.3 μg also significantly increased intercontraction intervals in the CYP-treated group. Intravenous or intrathecal administration of BAM8-22 did not change baseline pressure or maximum voiding pressure in the CYP-treated group.

CONCLUSIONS

These findings indicate that activation of SNSRs can suppress CYP-induced bladder overactivity, probably due to suppression of bladder afferent activity.

摘要

目的

研究激活感觉神经元特异性受体(SNSRs)对环磷酰胺(CYP)诱导的大鼠膀胱过度活动的影响。

方法

使用雌性Sprague-Dawley大鼠(235 - 258克)。大鼠腹腔注射CYP(200毫克/千克)或生理盐水(对照组)。在乌拉坦麻醉下,于注射CYP或生理盐水48小时后记录连续膀胱内压图(0.04毫升/分钟)。在建立稳定的排尿周期后,静脉内或鞘内给予选择性大鼠SNSR1激动剂牛肾上腺髓质8 - 22(BAM8 - 22)。

结果

与对照组相比,环磷酰胺治疗导致更高的基线压力和更短的收缩间期。在CYP治疗组中,静脉注射10、30和100微克/千克的BAM8 - 22显著增加了收缩间期。鞘内注射0.03、0.1和0.3微克的BAM8 - 22也显著增加了CYP治疗组的收缩间期。静脉或鞘内注射BAM8 - 22并未改变CYP治疗组的基线压力或最大排尿压力。

结论

这些发现表明,激活SNSRs可抑制CYP诱导的膀胱过度活动,可能是由于抑制了膀胱传入活动。

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