Izumi Kamo

Comparison of leak point pressure methods in an animal model of stress urinary incontinence

We compared three different methods of testing leak point pressure (LPP) in rats with or without the pudendal nerves and nerves to the iliococcygeus/pubococcygeus muscles transected: (1) sneeze induced with a whisker in the nostril (sneeze LPP), (2) manually increased abdominal pressure (Crede LPP), and (3) increased intravesical pressure using the vertical tilt table method (vertical tilt table LPP). In sham rats, passive intravesical pressure rises in Crede and vertical tilt table methods induced active urethral closure mechanisms that contributed to high LPPs (41.4 and 35.5xa0cmH2O, respectively), which were significantly reduced by nerve transection. During sneezing, leakage was observed in nerve-transected rats, but not in sham rats, indicating that sneezing can activate an additional urethral closure mechanism. Measuring LPP during sneezing or passive intravesical pressure rises in the vertical tilt table and Crede method seems to be useful for assessing the continence mechanisms under different stress conditions in rats.

A tissue‐engineered suburethral sling in an animal model of stress urinary incontinence

To create and evaluate the functional effects of a tissue‐engineered sling in an animal model of stress urinary incontinence (SUI).

Two kinds of urinary continence reflexes during abrupt elevation of intravesical pressure in rats.

Urethral closure mechanisms during abrupt elevation of intravesical pressure (Pves) were investigated. Middle urethral contractile responses were observed during sneezing and passive Pves rise for 120 sec. Both responses were decreased when somatic nerves innervating the external urethral sphincter and the pelvic floor muscles were transected. In contrast, while transection of both pelvic and hypogastric nerves had no effect during sneezing, urethral responses during passive Pves rise were totally abolished or partially reduced after transection of pelvic or hypogastric nerves, respectively. Electrical stimulation of the abdominal muscles for 1 sec elevated Pves, and Pves inducing fluid leakage from the urethral orifice was lowered after somatic or pelvic nerves were cut, while hypogastric nerve transection showed smaller effects. These results indicate that at least two kinds of urinary continence reflexes close the middle urethra; one is preprogrammed to close irrespective of bladder afferent activity, the other is triggered by bladder afferent activity. During momentary stress events lasting within 1 sec, the striated muscle mainly contributes to urethral closure, while during events lasting a relatively long period, like passive Pves rise for 120 sec, both striated and smooth muscles are related to the prevention of urinary incontinence.

Nerve Growth Factor, Endothelin and Spinal Cord Injury in Lower Urinary Tract Dysfunction

The lower urinary tract has two main functions: (i) storage and (ii) periodic expulsion of urine, which are regulated by a complex neural control system in the brain and lumbosacral spinal cord. Spinal cord injury at cervical or thoracic levels disrupts voluntary control of voiding, as well as the normal reflex pathways that coordinate bladder and sphincter function. Following an initial areflexic period, detrusor hyperreflexia and detrusor‐sphincter dyssynergia develop due to the plasticity of bladder afferent pathways and the unmasking of reflexes triggered by capsaicin‐sensitive C‐fiber bladder afferents. The plasticity is mediated in part by an increase in nerve growth factors released in the spinal cord and the peripheral target organs, as well as upregulated endogenous endothelin mechanisms.