Influences of Bilateral Hypogastric Nerve Transection on Voiding Dysfunction in the Rat with Spinal Cord Injury

Aims of Study Spinal cord injury (SCI) rostral to the lumbosacral level causes lower urinary tract dysfunction characterized by detrusor hyperreflexia, incontinence and un-coordinated bladder and external urethral sphincter (EUS) activity, termed detrusor-sphincter dyssynergia (DSD) [1]. DSD increases outlet resistance and induces high intravesical pressures during voiding that can damage the upper urinary tract. Thus, drug therapies or surgical procedures that diminish urethral resistance and/or intravesical pressure would be helpful in reducing urinary tract complications associated with DSD. Numerous studies have revealed that sympathetic efferent signals passing through the hypogastric nerve (HGN) and the lumbosacral sympathetic chain control the bladder neck (BN) and proximal urethra (PU) that form the internal urethral sphincter [2]. Excitatory sympathetic input to the BN/PU maintains closure of the outlet for urine during storage period. Therefore, it is presumed that reduction of urethral resistance to improve voiding can be induced by diminishing sympathetic transmission to the BN/PU by drug or surgical treatment. The present studies were conducted to determine whether bilateral section of HGNs, which provided the major sympathetic outflow to BN/PU [3], could improve voiding function by reducing urethral resistance in conscious female SCI rats.