AIMS: Bladder outlet obstruction (BOO) can mediate structural and functional detrusor changes, which can lead to bothersome lower urinary tract symptoms. We investigate if sacral nerve stimulation (SNS) can prevent these structural and functional changes in a rat model of BOO. METHODS: 24 female Sprague-Dawley rats (250 gm) were divided into 4 groups: control (CTRL), BOO, SNS, and both (BOO/SNS). BOO was achieved by partially occluding the proximal urethra. SNS involved stimulating the S1-S4 dorsal roots with a unipolar S1 lead, 8 hours daily. Urodynamics were performed at baseline and after 6 weeks. Bladders were harvested, stained, and scored for detrusor hypertrophy and fibrosis (scale = 1-5). RESULTS: BOO caused an increase in mean voiding pressure (P(det) = 35 +/- 2 mmHg vs. 23 +/- 1 mmHg, p = 0.02), an increase in mean bladder capacity (C = 1230 +/- 250 microl vs. 484 +/- 60 microl, p = 0.03), and a decrease in mean volume at first non-voiding contraction (67 +/- 16 microl vs. 110 +/- 24 microl, p = 0.02) compared to CTRL. Addition of SNS neither significantly affected P(det) (30 +/- 3 mm Hg vs. 35 +/- 2 mmHg, p = 0.2), nor C (630 +/- 90 microl vs. 1230 +/- 250 microl, p = 0.06) compared to BOO, but eliminated non-voiding contractions. Detrusor hypertrophy and fibrosis were both significantly greater in BOO vs. CTRL and vs. BOO/SNS. CONCLUSIONS: Partial BOO caused functional and structural changes in the rat bladder. SNS in obstructed rats prevents these alterations, without adversely affecting detrusor contractility. (c) 2010 Wiley-Liss, Inc.
AIMS: Bladder outlet obstruction (BOO) can mediate structural and functional detrusor changes, which can lead to bothersome lower urinary tract symptoms. We investigate if sacral nerve stimulation (SNS) can prevent these structural and functional changes in a rat model of BOO. METHODS: 24 female Sprague-Dawley rats (250 gm) were divided into 4 groups: control (CTRL), BOO, SNS, and both (BOO/SNS). BOO was achieved by partially occluding the proximal urethra. SNS involved stimulating the S1-S4 dorsal roots with a unipolar S1 lead, 8 hours daily. Urodynamics were performed at baseline and after 6 weeks. Bladders were harvested, stained, and scored for detrusor hypertrophy and fibrosis (scale = 1-5). RESULTS: BOO caused an increase in mean voiding pressure (P(det) = 35 +/- 2 mmHg vs. 23 +/- 1 mmHg, p = 0.02), an increase in mean bladder capacity (C = 1230 +/- 250 microl vs. 484 +/- 60 microl, p = 0.03), and a decrease in mean volume at first non-voiding contraction (67 +/- 16 microl vs. 110 +/- 24 microl, p = 0.02) compared to CTRL. Addition of SNS neither significantly affected P(det) (30 +/- 3 mm Hg vs. 35 +/- 2 mmHg, p = 0.2), nor C (630 +/- 90 microl vs. 1230 +/- 250 microl, p = 0.06) compared to BOO, but eliminated non-voiding contractions. Detrusor hypertrophy and fibrosis were both significantly greater in BOO vs. CTRL and vs. BOO/SNS. CONCLUSIONS: Partial BOO caused functional and structural changes in the rat bladder. SNS in obstructed rats prevents these alterations, without adversely affecting detrusor contractility. (c) 2010 Wiley-Liss, Inc.
Authors: Holly E Richter; Pamela Moalli; Cindy L Amundsen; Anna P Malykhina; Dennis Wallace; Rebecca Rogers; Deborah Myers; Maria Paraiso; Michael Albo; Haolin Shi; Tracy Nolen; Susie Meikle; R Ann Word Journal: J Urol Date: 2017-01-13 Impact factor: 7.450
Authors: Ranjana Jairam; Jamie Drossaerts; Tom Marcelissen; Gommert van Koeveringe; Desiree Vrijens; Philip van Kerrebroeck Journal: Urol Int Date: 2021-05-31 Impact factor: 1.934