Abstract

The aim of the study was to develop a new durable animal model (using rabbits) for anatomical-functional evaluation of urethral sphincter deficiency. A total of 40 New Zealand male rabbits, weighting 2.500 kg to 3.100 kg, were evaluated to develop an incontinent animal model. Thirty-two animals underwent urethrolysis and 8 animals received sham operation. Before and at 2, 4, 8 and 12 weeks after urethrolysis or sham operation, it was performed cystometry and leak point pressure (LPP) evaluation with different bladder distension volumes (10, 20, 30 mL). In each time point, 10 animals (8 from the study group and 2 from the sham group) were sacrificed to harvest the bladder and urethra. The samples were evaluated by H&E and Masson 's Trichrome to determine urethral morphology and collagen/smooth muscle density. Twelve weeks after urethrolysis, it was observed a significant decrease in LPP regardless the bladder volume (from 33.7 ± 6.6 to 12.8 ± 2.2 cmH₂O). The histological analysis evidenced a decrease of 22% in smooth muscle density with a proportional increase in the collagen, vessels and elastin density (p < 0.01). Transabdominal urethrolysis develops urethral sphincter insufficiency in rabbits, with significant decrease in LPP associated with decrease of smooth muscle fibers and increase of collagen density. This animal model can be used to test autologous cell therapy for stress urinary incontinence treatment.

Highlights

  • Stress urinary incontinence (SUI) is a high prevalent condition with great economic and quality of life impact [1]

  • Loss of adequate anatomic urethral support and intrinsic sphincter deficiency (ISD) are the two major components related to the development of stress urinary incontinence (SUI)

  • The lack of an ideal substance to use as bulking agent and the potential to urethral function regeneration by means of cell therapy and tissue engineering lead to studies based on cells transplantation into the urethral wall and rhabdosphincter [6,7,8]

Read more

Summary

Introduction

Stress urinary incontinence (SUI) is a high prevalent condition with great economic and quality of life impact [1]. Loss of adequate anatomic urethral support and intrinsic sphincter deficiency (ISD) are the two major components related to the development of stress urinary incontinence (SUI). The lack of an ideal substance to use as bulking agent and the potential to urethral function regeneration by means of cell therapy and tissue engineering lead to studies based on cells transplantation into the urethral wall and rhabdosphincter [6,7,8]. Such therapies are associated with major potential risks that should be extensively evaluated before clinical application

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call