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出生创伤大鼠模型中喷嚏诱导应激条件下主动尿道闭合机制的功能分析

Functional analysis of active urethral closure mechanisms under sneeze induced stress condition in a rat model of birth trauma.

作者信息

Kamo Izumi, Kaiho Yasuhiro, Canon Tracy W, Chancellor Michael B, de Groat William C, Prantil Rachelle L, Vorp David A, Yoshimura Naoki

机构信息

Department of Urology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA.

出版信息

J Urol. 2006 Dec;176(6 Pt 1):2711-5. doi: 10.1016/j.juro.2006.07.139.

Abstract

PURPOSE

We evaluated changes in the urethral closure mechanism under a sneeze induced stress condition in a rat model of birth trauma.

MATERIALS AND METHODS

Four days after vaginal distention induced by balloon catheter inflation in the vagina sneezing was induced while recording intravesical pressure with the rat under urethane anesthesia to evaluate sneeze induced leak point pressure, defined as the lowest pressure inducing fluid leakage from the urethral meatus during sneezing. Sneeze induced responses in the bladder and proximal or mid urethra were also measured using microtip transducer catheters.

RESULTS

In 5 sham operated rats no leakage was observed from the urethral meatus during sneezing, which produced an increase in intravesical pressure of up to 34 cm H(2)O. However, in 5 of 6 rats with vaginal distention leakage during sneezing was observed with a sneeze leak point pressure of 26.2 cm H(2)O. In the mid urethra microtip transducer catheters revealed that pressure increases during sneezing were greater than those in the bladder but they were significantly decreased in the 5 incontinent vaginal distention rats. However, sneeze induced responses at the proximal urethra, which were similar to those in the bladder, were not different in sham operated and incontinent vaginal distention rats.

CONCLUSIONS

Sneeze induced stress urinary incontinence in a rat model of birth trauma was caused by decreased active closure mechanisms at the mid urethra without affecting the passive transmission of abdominal pressure in the proximal urethra.

摘要

目的

我们在出生创伤大鼠模型中评估了喷嚏诱发应激条件下尿道闭合机制的变化。

材料与方法

在阴道内通过球囊导管充气诱导阴道扩张4天后,在乌拉坦麻醉下对大鼠进行喷嚏诱发,同时记录膀胱内压,以评估喷嚏诱发漏点压力,即喷嚏时导致尿道口漏液的最低压力。还使用微尖端换能器导管测量膀胱及尿道近端或中段的喷嚏诱发反应。

结果

在5只假手术大鼠中,喷嚏时尿道口未观察到漏液,膀胱内压升高至34 cm H₂O。然而,在6只阴道扩张大鼠中,有5只在喷嚏时出现漏液,喷嚏漏点压力为26.2 cm H₂O。在尿道中段,微尖端换能器导管显示喷嚏时压力升高大于膀胱,但在5只失禁的阴道扩张大鼠中显著降低。然而,尿道近端的喷嚏诱发反应与膀胱相似,在假手术大鼠和失禁的阴道扩张大鼠中无差异。

结论

出生创伤大鼠模型中喷嚏诱发的压力性尿失禁是由尿道中段主动闭合机制降低引起的,而不影响尿道近端腹压的被动传递。

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