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阴道扩张对雌性大鼠泌尿生殖器官血流及缺氧的影响。

Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat.

作者信息

Damaser M S, Whitbeck C, Chichester P, Levin R M

机构信息

Research Service, Hines Veterans Affairs Hospital, Hines, New York, USA.

出版信息

J Appl Physiol (1985). 2005 May;98(5):1884-90. doi: 10.1152/japplphysiol.01071.2004. Epub 2004 Dec 10.

Abstract

Vaginal delivery of children causes traumatic injury to tissues of the pelvic floor and is correlated with stress urinary incontinence; however, the exact mechanism of organ and tissue injury leading to incontinence development is unknown. The purpose of this project was to test the hypothesis that vaginal distension results in decreased blood flow to, and hypoxia of, the urogenital organs responsible for continence, which would suggest an ischemic and/or reperfusion mechanism of injury. Thirteen female rats underwent vaginal distension for 1 h. Thirteen age-matched rats were sham-distended controls. Blood flow to the bladder, urethra, and vagina were determined using a microsphere technique. Hypoxia of these organs was determined by immunohistochemistry. Blood flow to all three organs was significantly decreased just before release of vaginal distension. Bladder blood flow decreased further immediately after release of vaginal distension and continued to be significantly decreased 15 min after the release. Blood flow to both the urethra and vagina tripled immediately after release, inducing a rapid return to normal values. Vaginal distension resulted in extensive smooth muscle hypoxia of the bladder, as well as extensive hypoxia of the vaginal epithelium and urethral hypoxia. Bladders from sham-distended rats demonstrated urothelial hypoxia as well as focal hypoxic areas of the detrusor muscle. We have clearly demonstrated that vaginal distension results in decreased blood flow to, and hypoxia of, the bladder, urethra, and vagina, supportive of hypoxic injury as a possible mechanism of injury leading to stress urinary incontinence.

摘要

经阴道分娩会对盆底组织造成创伤性损伤,并与压力性尿失禁相关;然而,导致失禁发生的器官和组织损伤的确切机制尚不清楚。本项目的目的是检验以下假设:阴道扩张会导致负责控尿的泌尿生殖器官血流量减少和缺氧,这提示了一种缺血和/或再灌注损伤机制。13只雌性大鼠接受了1小时的阴道扩张。13只年龄匹配的大鼠作为假扩张对照组。使用微球技术测定膀胱、尿道和阴道的血流量。通过免疫组织化学测定这些器官的缺氧情况。在阴道扩张解除前,所有三个器官的血流量均显著下降。阴道扩张解除后,膀胱血流量立即进一步下降,并在解除后15分钟持续显著下降。尿道和阴道的血流量在解除后立即增加两倍,迅速恢复到正常水平。阴道扩张导致膀胱广泛的平滑肌缺氧,以及阴道上皮广泛缺氧和尿道缺氧。假扩张大鼠的膀胱显示尿路上皮缺氧以及逼尿肌的局灶性缺氧区域。我们已经清楚地证明,阴道扩张会导致膀胱、尿道和阴道的血流量减少和缺氧,支持缺氧损伤是导致压力性尿失禁的一种可能损伤机制。

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