Vulnerability of continence structures to injury by simulated childbirth

Author:

Phull Hardeep S.1,Pan Hui Q.1,Butler Robert S.2,Hansel Donna E.3456,Damaser Margot S.167

Affiliation:

1. Department of Biomedical Engineering, Lerner Research Institute,

2. Department of Quantitative Health Sciences,

3. Pathology and Laboratory Medicine Institute,

4. Taussig Cancer Institute,

5. Genomic Medicine Institute,

6. Glickman Urological and Kidney Institute, The Cleveland Clinic, Cleveland; and

7. Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, Ohio

Abstract

The goal of this study was to examine acute morphological changes, edema, muscle damage, inflammation, and hypoxia in urethral and vaginal tissues with increasing duration of vaginal distension (VD) in a rat model. Twenty-nine virgin Sprague-Dawley rats underwent VD under anesthesia with the use of a modified Foley catheter inserted into the vagina and filled with saline for 0, 1, 4, or 6 h. Control animals were anesthetized for 4 h without catheter placement. Urogenital organs were harvested after intracardiac perfusion of fixative. Tissues were embedded, sectioned, and stained with Masson's trichrome or hematoxylin and eosin stains. Regions of hypoxia were measured by hypoxyprobe-1 immunohistochemistry. Within 1 h of VD, the urethra became vertically elongated and displaced anteriorly. Edema was most prominent in the external urethral sphincter (EUS) and urethral/vaginal septum within 4 h of VD, while muscle disruption and fragmentation of the EUS occurred after 6 h. Inflammatory damage was characterized by the presence of polymorphonuclear leukocytes in vessels and tissues after 4 h of VD, with the greatest degree of infiltration occurring in the EUS. Hypoxia localized mostly to the vaginal lamina propria, urethral smooth muscle, and EUS within 4 h of VD. Increasing duration of VD caused progressively greater tissue edema, muscle damage, and morphological changes in the urethra and vagina. The EUS underwent the greatest insult, demonstrating its vulnerability to childbirth injury.

Publisher

American Physiological Society

Subject

Physiology

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