Phillip P. Smith MD, Christopher P. Smith, MD, Timothy B. Boone, MD, PhD, George T. Somogyi, MD, PhD, Scott Department of Urology, Baylor College of Medicine, Houston TX

Introduction: Normal voiding in the rat requires activation of the abdominal wall striated muscle during urine flow. This voiding-associated abdominal wall response (VAR) appears to be similar to the visceromotor response (VMR) to noxious visceral distension. Capsaicin-sensitive neuronal signaling is important in both nociception and normal voiding. The VMR is also sensitive to intravascular anesthetics and analgesics. We hypothesized that the voiding-associated abdominal wall activity would be altered by manipulations affecting the VMR and nociception. The aim of this study was to compare abdominal wall activation during voiding to the VMR by evaluating the cystometric and EMG responses to pharmacologic modulation of afferent signaling, and therefore further elucidate of the role of the VAR in normal voiding.

Methods: Female urethane-anesthetized SD rats, 250-300 g, were studied using a free-voiding technique which does not require instrumentation of the urethra or bladder during observation. Intercontraction interval, per-void volume, average flow rate, quantitative voiding-associated rectus abdominis EMG response, and hemodynamic parameters in rats treated with intravenous lidocaine (0.625 mg/kg/min and 2.5 mg/kg/min), c-fiber densensitization with subcutaneous capsaicin injection (25/50/50 mg), and urothelial TRPV-1 receptor desensitization with intravesical capsaicin (100 µM for 30 minutes) were compared to those in non-treated free-voiding rats.

Results: Intravenous lidocaine slightly decreased the intercontraction interval but did not alter any other voiding-associated parameter. Subcutaneous capsaicin preparation decreased the intercontraction interval by 62%. Intravesical capsaicin eliminated evidence of contractile voiding and increased the hemodynamic response. Vehicle and transurethral catheterization alone impaired voiding parameters, yielding decreased flow and decreased per-void volume, as well as enhancing the viscerovascular response, suggesting urethral obstruction. Average blood pressure was elevated in all treatment groups.

Conclusions: Voiding-associated abdominal wall activity (VAR) is a normal somatic response to a physiologic visceral function. We conclude that voiding-associated abdominal wall activity is predominantly an A delta neuronal response, and is the lowest threshold physiologic somatic response to visceral stimulation represented by the visceromotor response to noxious stimuli. The importance of the abdominal wall activation may be to provide a necessary increment of bladder voiding pressure, ensuring adequate urine flow into the mid-urethra during the critical pulsatile phase of rat voiding. If so, a positive feedback loop is established in which urine driven into the urethra activates afferents leading to continued VAR and pulsatile external sphincter activity, thus perpetuating the void until bladder volume is insufficient to maintain urine flow into the urethra. Activation of urethral afferents by transurethral catheter severely disturbs voiding. Normal rat voiding includes somatic striated muscle activation in response to visceral stimulation, and thus may be a model for human voiding dysfunction.

UroToday.com Coverage of SUFU 2007

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