OBJECTIVES: To characterize the voiding function in a transgenic adenocarcinoma of murine prostate (TRAMP) mouse of advanced age, because it might provide a useful model of slow-onset bladder outlet obstruction. Spontaneous death from urinary outlet obstruction occurs in the TRAMP mouse. METHODS: A metabolic cage without a fecal separation screen was placed above a precision balance that reported the mass of the excreta pan every 100 ms. A computational algorithm identified voids suitable for uroflow assessment from other excretory events. A series of images were obtained automatically before and during the excretory events. RESULTS: The TRAMP mouse displayed a pulsatile voiding pattern characterized by a reduction in uroflow, prolongation of voiding, and droplet formation at the tip of the prepuce. Postmortem histologic examination revealed gross enlargement of the prostate, a suburethral tumor, dilation of the lumen of the urethra, and proteinaceous debris in the urethra and bladder. CONCLUSIONS: The observed changes were consistent with urethral obstruction induced by prostate enlargement and/or suburethral tumor. Additional studies are required to ascertain whether prostate enlargement per se is sufficient to produce urethral obstruction in the TRAMP mouse. This transgenic mouse strain may provide a model of slow-onset outlet obstruction that is more representative of bladder outlet obstruction caused by benign prostatic hyperplasia than is the obstruction produced by urethral ligation.
OBJECTIVES: To characterize the voiding function in a transgenic adenocarcinoma of murine prostate (TRAMP) mouse of advanced age, because it might provide a useful model of slow-onset bladder outlet obstruction. Spontaneous death from urinary outlet obstruction occurs in the TRAMPmouse. METHODS: A metabolic cage without a fecal separation screen was placed above a precision balance that reported the mass of the excreta pan every 100 ms. A computational algorithm identified voids suitable for uroflow assessment from other excretory events. A series of images were obtained automatically before and during the excretory events. RESULTS: The TRAMPmouse displayed a pulsatile voiding pattern characterized by a reduction in uroflow, prolongation of voiding, and droplet formation at the tip of the prepuce. Postmortem histologic examination revealed gross enlargement of the prostate, a suburethral tumor, dilation of the lumen of the urethra, and proteinaceous debris in the urethra and bladder. CONCLUSIONS: The observed changes were consistent with urethral obstruction induced by prostate enlargement and/or suburethral tumor. Additional studies are required to ascertain whether prostate enlargement per se is sufficient to produce urethral obstruction in the TRAMPmouse. This transgenic mouse strain may provide a model of slow-onset outlet obstruction that is more representative of bladder outlet obstruction caused by benign prostatic hyperplasia than is the obstruction produced by urethral ligation.
Authors: Hannah Ruetten; Kyle A Wegner; Helen L Zhang; Peiqing Wang; Jaskiran Sandhu; Simran Sandhu; Brett Mueller; Zunyi Wang; Jill Macoska; Richard E Peterson; Dale E Bjorling; William A Ricke; Paul C Marker; Chad M Vezina Journal: Am J Physiol Renal Physiol Date: 2019-08-07
Authors: Tristan M Nicholson; Jalissa L Nguyen; Glen E Leverson; Julia A Taylor; Frederick S Vom Saal; Ronald W Wood; William A Ricke Journal: Am J Physiol Renal Physiol Date: 2018-07-18
Authors: Tristan M Nicholson; Emily A Ricke; Paul C Marker; Joseph M Miano; Robert D Mayer; Barry G Timms; Frederick S vom Saal; Ronald W Wood; William A Ricke Journal: Endocrinology Date: 2012-09-04 Impact factor: 4.736