Neuropeptide Y- and Vasoactive Intestinal Polypeptide-Containing Nerves in the Intrinsic External Urethral Sphincter in the Areflexic Bladder Compared to Detrusor-Sphincter Dyssynergia in Patients with Spinal Cord Injury

1987 ◽  
Vol 138 (4 Part 1) ◽  
pp. 888-892 ◽  
Author(s):  
P. Milner ◽  
R. Crowe ◽  
G. Burnstock ◽  
J.K. Light
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropeptide Y ◽  
Vasoactive Intestinal Polypeptide ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Detrusor Sphincter Dyssynergia ◽  
Cord Injury ◽  
Intestinal Polypeptide

scholarly journals α1D-Adrenoceptor blockade increases voiding efficiency by improving external urethral sphincter activity in rats with spinal cord injury

2016 ◽  
Vol 311 (5) ◽  
pp. R971-R978 ◽  
Author(s):  
Hirokazu Ishida ◽  
Hiroki Yamauchi ◽  
Hideaki Ito ◽  
Hironobu Akino ◽  
Osamu Yokoyama
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lower Urinary Tract Dysfunction ◽  
Urethral Sphincter ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Detrusor Sphincter Dyssynergia ◽  
Sphincter Electromyography ◽  
Sprague Dawley Rats ◽  
Cord Injury

Ideal therapy for lower urinary tract dysfunction in patients with spinal cord injury (SCI) should decrease detrusor overactivity, thereby promoting urine storage at low intravesical pressure and promoting efficient voiding at low pressure by decreasing detrusor-sphincter dyssynergia. Here we investigated blockade of various α-adrenoceptors to determine the subtype that was principally responsible for improving the voiding dysfunction. The effects of the intravenous α-blocker naftopidil, the α-blocker BMY 7378, and the α-blocker silodosin were evaluated using cystometrography and external urethral sphincter-electromyography (EMG) in decerebrated, unanesthetized female Sprague-Dawley rats with chronic SCI following transection at Th8. Parameters measured included the voided volume, residual volume, voiding efficiency, and burst and silent periods on EMG. Compared with values in decerebrated non-SCI rats, EMG of decerebrated SCI rats revealed more prominent tonic activity, significantly shorter periods of bursting activity, and a reduced ratio of the silent to active period during bursting. Compared with the value before drug administration (control), the voiding efficiency was significantly increased by naftopidil (1 and 3 mg/kg) (<0.05 each), and the burst (<0.01 and <0.05, respectively) and silent periods (<0.01 each) on EMG were significantly lengthened. BMY 7378 (1 mg/kg) significantly increased voiding efficiency and lengthened the burst periods (<0.05 each). Silodosin did not affect any parameters. These results suggest that α-blockade reduces the urethral resistance associated with detrusor-sphincter dyssynergia, thus improving voiding efficiency in SCI rats.

Activation of the external urethral sphincter central pattern generator by a 5-HT1A receptor agonist in rats with chronic spinal cord injury

2007 ◽  
Vol 292 (4) ◽  
pp. R1699-R1706 ◽  
Author(s):  
Paul C. Dolber ◽  
Baojun Gu ◽  
Xiaoyang Zhang ◽  
Matthew O. Fraser ◽  
Karl B. Thor ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Receptor Agonist ◽  
Bladder Capacity ◽  
Female Rats ◽  
Residual Volume ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Chronic Spinal Cord Injury ◽  
Cord Injury

We recently demonstrated that treatment with the 5-HT1A/7 receptor agonist [(R)-(+)-8-hydroxy-2-di-n-propylamino]tetralin (8-OH-DPAT) increases bladder capacity in chloralose-anesthetized female cats with chronic spinal cord injury. In the current study, we investigated the effects of 8-OH-DPAT on bladder capacity and external urethral sphincter (EUS) activity in urethane-anesthetized female rats (initial body mass 175–200 g) with chronic spinal cord injury (transsection at T10). Cystometric study took place 8–12 wk posttranssection. Intravesical pressure was monitored in urethane-anesthetized rats with a transvesical catheter, and EUS activity was assessed electromyographically. Spinal cord injury disrupts phasic activity of the EUS, resulting in decreased voiding efficiency and increased residual volume. 8-OH-DPAT induced a dose-dependent decrease in bladder capacity (the opposite of its effect in chronic spinal cord-injured cats) with an increase in micturition volume and decrease in residual volume resulting from improvement in voiding efficiency. The unexpected improvement in voiding efficiency can be explained by the 8-OH-DPAT-induced emergence of phasic EUS relaxation. Phasic EUS relaxation was also altered by 8-OH-DPAT in spinally intact rats, whereas the 5-HT1A receptor antagonist N-tert-butyl-3-[4-(2-methoxyphenyl)-piperazin-1-yl]-2-phenylpropanamide (WAY-100635), on its own, was without effect. It remains to be determined when phasic relaxation is restored after spinal cord injury, and indeed whether it is ever truly lost or is only temporarily separated from excitatory input.

Experience with Electromyography of the External Urethral Sphincter in Spinal Cord Injury Patients

1982 ◽  
Vol 127 (2) ◽  
pp. 272-276 ◽  
Author(s):  
Tomohiko Koyanagi ◽  
Katsuhisa Arikado ◽  
Tsuneo Takamatsu ◽  
Ichiro Tsuji
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Cord Injury

scholarly journals Spinal stimulation of the upper lumbar spinal cord modulates urethral sphincter activity in rats after spinal cord injury

2015 ◽  
Vol 308 (9) ◽  
pp. F1032-F1040 ◽  
Author(s):  
Edsel M. Abud ◽  
Ronaldo M. Ichiyama ◽  
Leif A. Havton ◽  
Huiyi H. Chang
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Receptor Agonist ◽  
Lumbar Spinal Cord ◽  
Urethral Sphincter ◽  
External Urethral Sphincter ◽  
Cord Injury ◽  
Urethral Resistance ◽  
Serotonergic Receptor ◽  
Lumbar Spinal

After spinal cord injury (SCI), the neurogenic bladder is observed to develop asynchronous bladder and external urethral sphincter (EUS) contractions in a condition known as detrusor-sphincter dyssnergia (DSD). Activation of the EUS spinal controlling center located at the upper lumbar spinal cord may contribute to reduce EUS dyssynergic contractions and decrease urethral resistance during voiding. However, this mechanism has not been well studied. This study aimed at evaluating the effects of epidural stimulation (EpS) over the spinal EUS controlling center (L3) in combination with a serotonergic receptor agonist on EUS relaxation in naive rats and chronic (6–8 wk) T8 SCI rats. Cystometrogram and EUS electromyography (EMG) were obtained before and after the intravenous administration of 5HT-1A receptor agonist and antagonist. The latency, duration, frequency, amplitude, and area under curve of EpS-evoked EUS EMG responses were analyzed. EpS on L3 evoked an inhibition of EUS tonic contraction and an excitation of EUS intermittent bursting/relaxation correlating with urine expulsion in intact rats. Combined with a 5HT-1A receptor agonist, EpS on L3 evoked a similar effect in chronic T8 SCI rats to reduce urethral contraction (resistance). This study examined the effect of facilitating the EUS spinal controlling center to switch between urine storage and voiding phases by using EpS and a serotonergic receptor agonist. This novel approach of applying EpS on the EUS controlling center modulates EUS contraction and relaxation as well as reduces urethral resistance during voiding in chronic SCI rats with DSD.

Sign in / Sign up

Export Citation Format

Share Document