Abstract

Purpose: To investigate the association between the maximum cystometric capacity (MCC) and other cystometric parameters in lumbar canal stenosis (LCS) rats. Material and Methods: One small hole was drilled at the fifth lumbar vertebral arch (Sham), and a rectangular piece of silicone rubber was then placed in the epidural space (LCS) of Wister rats. Two weeks after surgery, awake cystometry was performed. LCS rats were divided into three groups: Group A (n = 5, MCC 1.81 mL). Cystometric parameters were investigated in sham and LCS groups. Results: MCC did not significantly correlate to the frequency of non-voiding contractions (NVCs), voided volume (VV), or maximum intravesical pressure during voiding (Pmax), but significantly positively correlated to postvoid residual urine volume (PVR) and residual urine rate (RUR) (Spearman’s correlation coefficients (ρ) = 0.8973 (p < 0.0001) and 0.4915 (p = 0.0068), respectively). Compared with the sham rats, LCS rats in each group revealed significantly smaller VV, larger RUR, and lower Pmax. On the other hand, among LCS rats, VV, RUR, and Pmax were not significantly different. The frequency of NVCs in each LCS group was not significantly different from that in sham-operated rats (Tukey-Kramer’s HSD test). However, a Jonckheere-Terpstra trend test revealed a significant trend toward higher NVCs in the order of sham, Groups C, B, and A (p = 0.036). Conclusions: LCS rats showed the same degree of detrusor underactivity regardless of MCC. NVCs did not significantly increase in LCS rats with decreased MCC, but the trend toward higher NVCs with smaller MCC was significant.

Highlights

  • A recent clinical study demonstrated that underactive bladder (UAB) could be preceded by overactive bladder (OAB) which is regarded as a compensatory mechanism for decreased shortening velocity [1]

  • In this study we investigated whether maximum cystometric capacity (MCC) was increased in lumbar canal stenosis (LCS) rats

  • We found that MCC in LCS rats was not always significantly larger than that in sham rats

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Summary

Introduction

A recent clinical study demonstrated that underactive bladder (UAB) could be preceded by overactive bladder (OAB) which is regarded as a compensatory mechanism for decreased shortening velocity [1]. Nomiya et al investigated bladder function in an atherosclerosis rat model that was induced by endothelial injury of the internal iliac artery with a high cholesterol diet [2]. These rats manifested an OAB phenotype in a metabolic cage study and on awake cystometry. In vivo muscle strip studies showed impaired detrusor contractility. Based on these studies, some researchers proposed the existence of an “OAB to UAB transition” [3]-[6]

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