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Objective: To evaluate the effectiveness of 3D NerveVIEW sequence with gadolinium contrast on the visualization of pelvic nerves and their branches compared to that without contrast. Methods: Participants were scanned twice using 3D NerveVIEW sequence with and without gadolinium contrast to acquire pelvic nerve images. The signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR) and contrast ratio of the nerves were calculated and compared to determine the quality of images. To subjectively assess, using a 3-point scale, branch nerves critical to therapeutic decision-making, including the pelvic splanchnic nerve and pelvic plexus, the superior gluteal nerve, and the pudendal nerve. Results: In the 32 eligible participants after using contrast, the CNRs of the images of nerve-to-bone and nerve-to-vessel significantly increased (p < 0.05). The CR of the images with contrast of all nerve-to-surrounding tissues (i.e., bone, muscle, blood vessels, and fat) were also found significantly higher (p < 0.05). The assessment of observers also shows higher scores for images with contrast compared to images without contrast. Conclusion: The 3D NerveVIEW sequence combined with gadolinium contrast improved vascular suppression, increased the contrast between pelvic nerves and surrounding tissue, and enhanced the visualization of nerves and their branches. This study may be helpful for the technically challenging preoperative planning of pelvic diseases surgery. [ABSTRACT FROM AUTHOR]

We have demonstrated in canines that somatic nerve transfer to vesical branches of the inferior hypogastric plexus (IHP) can be used for bladder reinnervation after spinal root injury. Yet, the complex anatomy of the IHP hinders the clinical application of this repair strategy. Here, using human cadavers, we clarify the spatial relationships of the vesical branches of the IHP and nearby pelvic ganglia, with the ureteral orifice of the bladder. Forty-four pelvic regions were examined in 30 human cadavers. Gross post-mortem and intra-operative approaches (open anterior abdominal, manual laparoscopic, and robot-assisted) were used. Nerve branch distances and diameters were measured after thorough visual inspection and gentle dissection, so as to not distort tissue. The IHP had between 1 to 4 vesical branches (2.33 ± 0.72, mean ± SD) with average diameters of 0.51 ± 0.06 mm. Vesical branches from the IHP arose from a grossly visible pelvic ganglion in 93% of cases (confirmed histologically). The pelvic ganglion was typically located 7.11 ± 6.11 mm posterolateral to the ureteral orifice in 69% of specimens. With this in-depth characterization, vesical branches from the IHP can be safely located both posterolateral to the ureteral orifice and emanating from a more proximal ganglionic enlargement during surgical procedures. [ABSTRACT FROM AUTHOR]

Copyright of Autonomic Nervous System / Jiritsu Shinkei is the property of Japan Society of Neurovegetative Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: This study evaluated the visualization of the pelvic nerves using magnetic resonance imaging (MRI) combined with computed tomography (CT) to synthesize three-dimensional (3D) reconstruction images of the pelvic organs. Methods: The CT and MRI scans were performed for patients with rectal cancer who underwent surgery. The out-of-phase image of LAVA-Flex was used to identify the pelvic nerves. The images of the pelvic nerves were extracted from the MRI scans, and those of the arteries and rectum and pelvis were extracted from the CT scans. Each extracted organ image was used to synthesize 3D reconstruction images. Results: The MRI scan allowed adequate visualization of the pelvic splanchnic nerves, inferior hypogastric plexus, and obturator nerves. The comparison of 3D reconstruction images and intraoperative findings showed matched images. Conclusion: We visualized the pelvic nerves using MRI and synthesized 3D reconstruction images of the pelvic organs. Preoperative confirmation of the location of the pelvic organs is important to prevent unanticipated injury during rectal cancer surgery. [ABSTRACT FROM AUTHOR]

Sexual dysfunction can be caused by impaired neurotransmission from the peripheral to the central nervous system. Therefore, it is important to evaluate the input of sensory information from the peripheral genital area and investigate the control mechanisms in the spinal cord to clarify the pathological basis of sensory abnormalities in the genital area. However, an in vivo evaluation system for the spinal cord–penile neurotransmission mechanism has not yet been developed. Here, urethane-anesthetized rats were used to evaluate neuronal firing induced by innocuous or nociceptive stimulation of the penis using extracellular recording or patch-clamp techniques in the lumbosacral spinal dorsal horn and electrophysiological evaluation in the peripheral pelvic nerves. As a result, innocuous and nociceptive stimuli-evoked neuronal firing was successfully recorded in the deep and superficial spinal dorsal horns, respectively. The innocuous stimuli-evoked nerve firing was also recorded in the pelvic nerve. These firings were suppressed by lidocaine. To the best of our knowledge, this is the first report of a successful quantitative evaluation of penile stimuli-evoked neuronal firing. This method is not only useful for analyzing the pathological basis of spinal cord–penile neurotransmission in sexual dysfunction but also provides a useful evaluation system in the search for new treatments. [ABSTRACT FROM AUTHOR]

Purpose: The urinary bladder generates phasic contractions via action potentials generated in pre- and then postganglionic neurons. Whilst the frequency-dependence of postganglionic neurons to generate contractions has been quantified, the dynamic range of preganglionic neurons is less clear and if intramural ganglia exert frequency-dependent modulation of transmission between pre- and postganglionic neurons. The phosphodiesterase type 5 inhibitor sildenafil reduces neurotransmitter release from postganglionic fibres to detrusor smooth muscle and an additional question was if there was also a preganglionic action. This study aimed to compare the frequency range of bladder contractile activation by pre- and postganglionic stimulation in pig and rat bladders and if sildenafil exerted additional preganglionic actions. Methods: An arterially-perfused ex vivo pig bladder preparation was used for preganglionic (pelvic nerve) and mixed preand postganglionic (direct bladder wall) stimulation at 36°C and postganglionic mediated contractions achieved by field-stimulation of in vitro isolated detrusor strips. With rats, pelvic nerve stimulation was carried out in vivo and postganglionic stimulation also with isolated detrusor strips. Results: All contractions were abolished by 2% lignocaine indicating they are nerve-mediated. Stimulation targets were verified with hexamethonium that completely abolished pelvic nerve responses by had no effect on detrusor strips; responses to mixed bladder wall stimulation were partially reduced. The frequency-dependence of contractile activation was similar whether by pre- or postganglionic stimulation in both pigs and rats. Sildenafil reduced contractions to preganglionic stimulation significantly more than to postganglionic stimulation. Mixed pre- and postganglionic stimulation were reduced by an intermediate extent. Conclusions: Intramural ganglia offer no frequency-dependent modulation under the experimental conditions used here and the sildenafil data are consistent with multiple sites of action underlying generation of bladder contractions. A translational aspect of these findings is discussed in terms of setting stimulation parameters for neuromodulation protocols. [ABSTRACT FROM AUTHOR]

Selective electrical stimulation of the pudendal nerve exhibits promise as a potential therapy for treating overactive bladder (OAB) across species (rats, cats, and humans). More recently, pelvic nerve (PelN) stimulation was demonstrated to improve cystometric bladder capacity in a PGE2 rat model of OAB. However, PelN stimulation in humans or in an animal model that is more closely related to humans has not been explored. Therefore, our objective was to quantify the effects of PGE2 and PelN stimulation in the cat. Acute cystometry experiments were conducted in 14 α-chloralose-anesthetized adult, neurologically intact female cats. Intravesical PGE2 decreased bladder capacity, residual volume, threshold contraction pressure, and mean contraction pressure. PelN stimulation reversed the PGE2-induced decrease in bladder capacity and increased evoked external urethral sphincter electromyographic activity without influencing voiding efficiency. The increases in bladder capacity generated by PelN stimulation were similar in the rat and cat, but the stimulation parameters to achieve this effect differed (threshold amplitude at 10 Hz in the rat vs. twice threshold amplitude at 1 Hz in the cat). These results highlight the potential of PGE2 as a model of OAB and provide further evidence that PelN stimulation is a promising approach for the treatment of OAB symptoms. [ABSTRACT FROM AUTHOR]

Objectives: To create a rat model for neurogenic detrusor underactivity (DU) by bilateral pelvic nerve crush injury (BPNI) and to study temporal changes in detrusor contractility and morphology. Materials and Methods: Male Sprague‐Dawley rats were subjected to BPNI or sham surgery and evaluated at 1, 3 and 9 weeks after surgery. Bladder function was determined in vivo by awake cystometry, micturition pattern analysis, and 24‐h urine collection. Bladders were harvested for in vitro pharmacological investigation by isometric tension recording. Bladders and major pelvic ganglia were investigated by quantitative reverse transcription‐polymerase chain reaction and histochemistry. Results: Overflow incontinence was observed at 1 week after BPNI. At 3 and 9 weeks after BPNI, rats showed a bladder phenotype characteristic for DU with increased post‐void residual urine volumes, reduced voiding efficiencies, and lower maximum pressures. In isolated bladder strips, contractile responses to KCl, carbachol, and α,β‐methylene adenosine 5′‐triphosphate (α,β‐mATP) were preserved. On the other hand, neural‐induced contractility was reduced after BPNI, in line with reduced expression of protein gene product 9.5 and choline acetyltransferase in the major pelvic ganglion at 1 week after BPNI. The bladder‐to‐body weight ratio and detrusor thickness increased after BPNI, indicating detrusor hypertrophy to compensate for the reduced neural input. Conclusions: BPNI induces a rat model for neurogenic DU. In this model, the detrusor maintains its contractility but denervation of the detrusor was observed. [ABSTRACT FROM AUTHOR]

Female Wistar rats were instrumented to record bladder pressure and to stimulate the left pelvic nerve. Repeated voids were induced by continuous infusion of saline into the bladder (11.2 ml/h) via a T-piece in the line to the bladder catheter. In each animal tested (n = 6) high frequency pelvic nerve stimulation (1-3 kHz, 1-2 mA sinusoidal waveform for 60 s) applied within 2 s of the onset of a sharp rise in bladder pressure signaling an imminent void was able to inhibit micturition. Voiding was modulated in three ways: (1) Suppression of voiding (four rats, n = 13 trials). No fluid output or a very small volume of fluid expelled (<15% of the volume expected based on the mean of the previous 2 or 3 voids). Voiding suppressed for the entirety of the stimulation period (60 s) and resumed within 37 s of stopping stimulation. (2) Void deferred (four rats, n = 6 trials). The imminent void was suppressed (no fluid expelled) but a void occurred later in the stimulation period (12-44 s, mean 24.5 ± 5.2 s after the onset of the stimulation). (3) Reduction in voided volume (five rats, n = 20 trials). Voiding took place but the volume of fluid voided was 15-80% (range 21.8-77.8%, mean 45.3 ± 3.6%) of the volume expected from the mean of the preceding two or three voids. Spontaneous voiding resumed within 5 min of stopping stimulation. Stimulation during the filling phase in between voids had no effect. The experiments demonstrate that conditional high frequency stimulation of the pelvic nerve started at the onset of an imminent void can inhibit voiding. The effect was rapidly reversible and was not accompanied by any adverse behavioral side effects. [ABSTRACT FROM AUTHOR]

Aim To quantify the effects of pulsed radiofrequency (PRF) electrical stimulations of the pudendal and pelvic nerves on the bladder function of rats with detrusor overactivity. Methods All rats were pretreated with a continuous transvesical infusion of 0.5% acetic acid (AA) for inducing detrusor overactivity. Intravesical pressure was recorded using cysometrography (CMG) during the continuous transvesical infusion to examine the effects of PRF electrical stimulation of the pudendal and pelvic nerves individually. In addition, the activity of caspase-3, an apoptosis marker, in the pelvic nerve was examined to evaluate the impact of PRF on nerve injury. Results According to the first CMG recording, AA treatment significantly reduced bladder capacity (BC) and intercontraction interval (ICI) to 65% and 66% of the corresponding control values, respectively. Subsequently, PRF electrical stimulation of the pelvic nerve inhibited AA-induced detrusor overactivity and significantly increased BC to approximately 102-110% and ICI to 79-92%; these effects persisted for at least 4 h. Furthermore, PRF did not cause significant neural damage to the target stimulated nerves, as demonstrated by caspase-3 activity. Conclusion PRF electrical stimulation of pelvic nerves exerted a long-lasting effect of suppressing AA-induced detrusor overactivity. This modality can be used as an alternative approach for improving bladder continence in patients with overactive bladder syndrome. [ABSTRACT FROM AUTHOR]

Overactive bladder (OAB) syndrome is a highly prevalent condition that may lead to medical complications and decreased quality of life. Emerging therapies focusing on selective electrical stimulation of peripheral nerves associated with lower urinary tract function may provide improved efficacy and reduced side effects compared with sacral neuromodulation for the treatment of OAB symptoms. Prior studies investigating the effects of pelvic nerve (PelN) stimulation on lower urinary tract function were focused on promoting bladder contractions, and it is unclear whether selective stimulation of the PelN would be beneficial for the treatment of OAB. Therefore our motivation was to test the hypothesis that PelN stimulation would increase bladder capacity in the prostaglandin E2 (PGE2) rat model of OAB. Cystometry experiments were conducted in 17 urethane-anesthetized female SpragueDawley rats. The effects of intravesical PGE2 vs. vehicle and PelN stimulation after intravesical PGE2 on cystometric parameters were quantified. Intravesical infusion of PGE2 resulted in decreased bladder capacity and increased voiding efficiency without a change in bladder contraction area under the curve, maximum contraction pressure, or contraction duration. Bladder capacity was also significantly decreased compared with vehicle (1% ethanol in saline) confirming that the change in bladder capacity was mediated by PGE2. PelN stimulation reversed the PGE2-induced change in bladder capacity and increased the external urethral sphincter electromyogram activity at a specific stimulation condition (amplitude of 1.0 times threshold at 10 Hz). These results confirm that the urodynamic changes reported in conscious rats are also observed under urethane anesthesia and that PelN stimulation is a novel and promising approach for the treatment of the symptoms of OAB. [ABSTRACT FROM AUTHOR]

Urge Urinary Incontinence: "a sudden and uncontrollable desire to void which is impossible to defer" is extremely common and considered the most bothersome of lower urinary tract conditions. Current treatments rely on pharmacological, neuromodulatory, and neurotoxicological approaches to manage the disorder, by reducing the excitability of the bladder muscle. However, some patients remain refractory to treatment. An alternative approach would be to temporarily suppress activity of the micturition control circuitry at the time of need i.e., urgency. In this study we investigated, in a rat model, the utility of high frequency pelvic nerve stimulation to produce a rapid onset, reversible suppression of voiding. In urethane-anesthetized rats periodic voiding was induced by continuous infusion of saline into the bladder whilst recording bladder pressure and electrical activity from the external urethral sphincter (EUS). High frequency (1-3 kHz), sinusoidal pelvic nerve stimulation initiated at the onset of the sharp rise in bladder pressure signaling an imminent void aborted the detrusor contraction. Urine output was suppressed and tone in the EUS increased. Stimulating the right or left nerve was equally effective. The effect was rapid in onset, reversible, and reproducible and evoked only minimal "off target" side effects on blood pressure, heart rate, respiration, uterine pressure, or rectal pressure. Transient contraction of abdominal wall was observed in some animals. Stimulation applied during the filling phase evoked a small, transient rise in bladder pressure and increased tonic activity in the EUS, but no urine output. Suppression of micturition persisted after section of the contralateral pelvic nerve or after ligation of the nerve distal to the electrode cuff on the ipsilateral side. We conclude that high frequency pelvic nerve stimulation initiated at the onset of an imminent void provides a potential means to control urinary continence. [ABSTRACT FROM AUTHOR]

Background: Mechanosensitive afferents innervating the bladder increase their firing rate as the bladder fills and pressure rises. However, the relationship between afferent firing rates and intravesical pressure is not a simple linear one. Firing rate responses to pressure can differ depending on prior activity, demonstrating hysteresis in the system. Though this hysteresis has been commented on in published literature, it has not been quantified.Results: Sixty-six bladder afferents recorded from sacral dorsal root ganglia in five alpha-chloralose anesthetized felines were identified based on their characteristic responses to pressure (correlation coefficient ≥ 0.2) during saline infusion (2 ml/min). For saline infusion trials, we calculated a maximum hysteresis ratio between the firing rate difference at each pressure and the overall firing rate range (or Hmax) of 0.86 ± 0.09 (mean ± standard deviation) and mean hysteresis ratio (or Hmean) of 0.52 ± 0.13 (n = 46 afferents). For isovolumetric trials in two experiments (n = 33 afferents) Hmax was 0.72 ± 0.14 and Hmean was 0.40 ± 0.14.Conclusions: A comprehensive state model that integrates these hysteresis parameters to determine the bladder state may improve upon existing neuroprostheses for bladder control. [ABSTRACT FROM AUTHOR]

Background: Glucagon-like peptide 1 (GLP-1) analogs protect a variety of cell types against oxidative damage and vascular and neuronal injury via binding to GLP-1 receptors. This study aimed to investigate the effects of the GLP-1 analogs exendin-4 and liraglutide on cerebral blood flow, reactive oxygen species production, expression of oxidative stress-related proteins, cognition, and pelvic sympathetic nerve-mediated bladder contraction after middle cerebral artery occlusion (MCAO) injury in the db/db mouse model of diabetes.Results: Sixty minutes of MCAO increased blood and brain reactive oxygen species counts in male db/db mice, as revealed by dihydroethidium staining. MCAO also increased nuclear factor-κB and intercellular adhesion molecule-1 expression and decreased cerebral microcirculation. These effects were attenuated by treatment with exendin-4 or liraglutide. MCAO did not affect basal levels of phosphorylated Akt (p-Akt) or endothelial nitric oxide synthase (p-eNOS); however, exendin-4 and liraglutide treatments significantly enhanced p-Akt and p-eNOS levels, indicating activation of the p-Akt/p-eNOS signaling pathway. MCAO-induced motor and cognitive deficits and micturition dysfunction, indicated by reduced pelvic nerve-mediated voiding contractions and increased nonvoiding contractions, were also partially attenuated by exendin-4 treatment.Conclusions: The above data indicate that treatment with GLP-1 agonists exerts protective effects against oxidative, inflammatory, and apoptotic damage in brain areas that control parasympathetic/pelvic nerve-mediated voiding contractions and cognitive and motor behaviors in a diabetic mouse model. [ABSTRACT FROM AUTHOR]

Aims The search for new animal models to investigate both efferent and afferent levels of the micturition reflex, to better understand urinary dysfunctions, is of great importance. Therefore in this study we developed and characterized, by comparisons with a conventional whole bladder model, a novel in situ model. Methods The urinary bladder was carefully prepared and separated, via a midline incision, into two halves all the way to the urethra in pentobarbitone and medetomidine anesthetized male rats. The separated bladder halves (with no direct connection) were immobilized with ligatures to the underlying tissue. The tension could thereafter be recorded at one side, while the other half was occasionally stretched in order to evoke an afferent signal. Also, injections of ATP and methacholine and electric nerve stimulation were employed. Results Ipsilateral stretch of 30 and 50 mN induced a force-dependent contractile response on the contralateral side. Moreover, electrical stimulation of efferent pelvic nerve fibers, and intravenous injections of methacholine and ATP, evoked dose-dependent contractions, resembling responses observed in the whole bladder model. Here, the threshold frequency at electrical stimulation of the efferent fibers was <2 Hz and the maximum response appeared at 10-20 Hz, while afferent stimulation had a threshold of 5-10 Hz with the maximum response at 40 Hz. Conclusions In the current study we show that stimulation of afferents at one side of the bladder induces, via impulses from the central nervous system, contractions from the other side. This novel model enables quantitative comparisons of changes occurring within the micturition reflex arc in bladder disorders. Neurourol. Urodynam. 33:550-557, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background/Aims: Colonic peristalsis is mainly regulated via intrinsic neurons in guinea pigs. However, autonomic regulation of colonic motility is poorly understood. We explored a guinea pig model for the study of extrinsic nerve effects on the distal colon. Methods: Guinea pigs were sacrificed, their distal colons isolated, preserving pelvic nerves (PN) and inferior mesenteric ganglia (IMG), and placed in a tissue bath. Fecal pellet propagation was conducted during PN and IMG stimulation at 10 Hz, 0.5 ms and 5 V. Distal colon was connected to a closed circuit system, and colonic motor responses were measured during PN and IMG stimulation. Results: PN stimulation increased pellet velocity to 24.6 ± 0.7 mm/sec (n = 20), while IMG stimulation decreased it to 2.0 ± 0.2 mm/sec (n = 12), compared to controls (13.0 ± 0.7 mm/sec, P < 0.01). In closed circuit experiments, PN stimulation increased the intraluminal pressure, which was abolished by atropine (10-6 M) and hexamethonium (10-4 M). PN stimulation reduced the incidence of non-coordinated contractions induced by NG-nitro-L-arginine methyl ester (L-NAME; 10-4 M). IMG stimulation attenuated intraluminal pressure increase, which was partially reversed by alpha-2 adrenoceptor antagonist (yohimbine; 10-6 M). Conclusions: PN and IMG input determine speed of pellet progression and peristaltic reflex of the guinea pig distal colon. The stimulatory effects of PN involve nicotinic, muscarinic and nitrergic pathways. The inhibitory effects of IMG stimulation involve alpha-2 adrenoceptors. [ABSTRACT FROM AUTHOR]

The urethrogenital reflex (UGR) is used as a surrogate model of the autonomic and somatic nerve and muscle activity that accompanies ejaculation. The UGR is evoked by distension of the urethra and activation of penile afferents. The current study compares two methods of elevating urethral intraluminal pressure in spinalized, anesthetized male Sprague-Dawley rats (n = 60). The first method, penile extension UGR, involves extracting the penis from the foreskin, so that urethral pressure rises due to a natural anatomical flexure in the penis. The second method, penile clamping UGR, involves penile extension UGR with the addition of clamping of the glans penis. Groups of animals were prepared that either received no additional treatment, surgical shams, or received bilateral nerve cuts (4 nerve cut groups): either the pudendal sensory nerve branch (SbPN), the pelvic nerves, the hypogastric nerves, or all three nerves. Penile clamping UGR was characterized by multiple bursts, monitored by electromyography (EMG) of the bulbospongiosus muscle (BSM) accompanied by elevations in urethral pressure. The penile clamping UGR activity declined across multiple trials and eventually resulted in only a single BSM burst, indicating desensitization. In contrast, the penile extension UGR, without penile clamping, evoked only a single BSM EMG burst that showed no desensitization. Thus, the UGR is composed of two BSM patterns: an initial single burst, termed urethrobulbospongiosus (UBS) reflex and a subsequent multiple bursting pattern (termed ejaculation-like response, ELR) that was only induced with penile clamping urethral occlusion. Transection of the SbPN eliminated the ELR in the penile clamping model, but the single UBS reflex remained in both the clamping and extension models. Pelvic nerve (PelN) transection increased the threshold for inducing BSM activation with both methods of occlusion but actually unmasked an ELR in the penile extension method. Hypogastric nerve (HgN) cuts did not significantly alter any parameter. Transection of all three nerves eliminated BSM activation completely. In conclusion, penile clamping occlusion recruits penile and urethral primary afferent fibers that are necessary for an ELR. Urethral distension without significant penile afferent activation recruits urethral primary afferent fibers carried in either the pelvic or pudendal nerve that are necessary for the single-burst UBS reflex. [ABSTRACT FROM AUTHOR]

This study investigates whether signals obtained from an implantable pressure sensor placed in the urinary bladder wall could be used to detect the onset of bladder contractions. The sensor assembly was custom made using a small piezoresistive sensor die. The die was mounted on ceramic substrate (8 mm × 8 mm) and encapsulated in silicone by a two-part moulding process. The final sensor was lens shaped with a diameter of 13.6 mm and height of 2.0 mm. Experiments were performed in six pigs that had one or more sensors placed in the bladder wall. An external reference sensor was used to simultaneously monitor intravesical pressure via a transurethral catheter. Bladder contractions were evoked by unilateral electrical stimulation of the pelvic nerve. Onset latency was computed using both signals. In addition, the correlation between wall pressure and intravesical pressure was calculated. On average, the onset latency was -307 ms using the wall sensors compared to the intravesical pressure, i.e., the detection occurred earlier using the wall sensors than the intravesical sensor. In 91 of 114 recordings the correlation coefficient was above 0.90. In conclusion, the implantable sensor performs similar to the reference sensor when used to detect the onset of bladder contractions. [ABSTRACT FROM AUTHOR]

Introduction. Injury to pelvic sympathetic and parasympathetic nerves from surgical and obstetrical trauma has long been cited as a cause for abnormal colorectal motility in humans. Using a rat model, acute transaction of these extrinsic nerves has been shown to effect colorectal motility. The aim of this study is to determine in a rat model how transection of these extrinsic nerves affects colonic transit over time. Methods. Eighty-two Sprague--Dawley rats underwent placement of a tunneled catheter into the proximal colon. Bilateral hypogastric, pelvic nerves (HGN and PN) or both were transected in 66 rats. The remaining 16 rats received a sham operation. Colonic transit was evaluated at postoperative days (PODs) 1, 3, and 7 by injecting and calculating the geometric center (GC) of the distribution of 51Cr after 3 h of propagation. Results. At POD 1, transection of PNs significantly delayed colonic transit (GC == 4.9, p < 0.05), while transection of HGNs (GC == 8.5, p < 0.05) or transection of both nerves (GC == 7.8, p < 0.05) significantly accelerated colonic transit, when compared with sham operation (GC == 6.0). A significant trend toward recovery was noted in both the HGN and PN transection groups at POD 7. Conclusions. Damage to the extrinsic sympathetic and/or parasympathetic PNs affects colonic transit acutely. These changes in large bowel motor function normalize over time implicating a compensatory mechanism within the bowel itself. [ABSTRACT FROM AUTHOR]

It is well-established that cyclophosphamide (CYP) can sensitize the pelvic afferent nerve arising from the urinary bladder and therefore induce suprapubic pain. To test the possibility that CYP might mediate the development of visceral hypereflexia/hyperalgesia by facilitating spinal activity-dependent neural plasticity, we compared the pelvic-urethra reflex activity and spinal N-methyl-d-aspartate receptor NR2B subunit (NR2B) phosphorylation in rats treated with vehicle solution and CYP. Compared with vehicle solution, when accompanied by upregulation of phosphorylated NR2B expression in the lumbosacral (L6-S2) dorsal horn, CYP increased the evoked spikes in spinal reflex potentiation induced by repetitive stimulation (1 stimulation/1 s). Moreover, intraperitoneal pretreatments with NG-nitro-l-arginine methyl ester and roscovitine, nitric oxide synthase and cyclin-dependent protein kinase 5 (Cdk5) antagonists, respectively, overwrote CYP-enhanced reflex potentiation and NR2B phosphorylation. When compared with the untreated group, the treatment with small-interfering RNA of NR2B, which decreased the expression of NR2B expression, abolished CYP-dependent reflex facilitation and spinal NR2B phosphorylation. These results suggested that CYP might facilitate spinal reflex potentiation mediated by N-methyl-d-aspartate receptors and participate in the development of visceral hypereflexia/hyperalgesia through nitric oxide- and Cdk5-dependent NR2B phosphorylation at the lumbosacral dorsal horn. [ABSTRACT FROM AUTHOR]

Background Several disease processes of the colon and rectum, including constipation and incontinence, have been associated with abnormalities of the autonomic nervous system. However, the autonomic innervation to the colon and rectum are not fully understood. The aims of this study were to investigate the effect of stimulation of vagus nerves, pelvic nerves (PN) and hypogastric nerves (HGN) on colorectal motility in rats. Methods Four strain gauge transducers were implanted on the proximal colon, mid colon, distal colon and rectum to record circular muscle contractions in rats. Electrical stimulation was administered to the efferent distal ends of the cervical vagus nerve, PN and HGN. Motility index (MI) was evaluated before and during stimulation. Key Results Electrical stimulation (5–20 Hz) of the cervical vagus elicited significant contractions in the mid colon and distal colon, whereas less pronounced contractions were observed in the proximal colon. Pelvic nerves stimulation elicited significant contractions in the rectum as well as the mid colon and distal colon. Atropine treatment almost completely abolished the contractions induced by vagus nerve and PN stimulation. Hypogastric nerves stimulation caused relaxations in the rectum, mid colon and distal colon. The relaxations in response to HGN stimulation were abolished by propranolol. Conclusions & Inferences Vagal innervation extends to the distal colon, while the PN has projections in the distribution of the rectum through the mid colon. This suggests a pattern of dual parasympathetic innervation in the left colon. Parasympathetic fibers regulate colorectal contractions via muscarinic receptors. The HGN mainly regulates colorectal relaxations via beta-adrenoceptors. [ABSTRACT FROM AUTHOR]

Studies in humans and rodents suggest that colon inflammation promotes urinary bladder hypersensitivity and, conversely, that cystitis contributes to colon hypersensitivity, events referred to as cross-organ sensitization. To investigate a potential peripheral mechanism, we examined whether cystitis alters the sensitivity of pelvic nerve cobrectal afferents. Male C57BL/6 mice were treated with cyclophosphamide (CYP) or saline, and the mechanosensitive properties of single afferent fibers innervating the colorectum were studied with an in vitro preparation. In addition, mechanosensitive receptive endings were exposed to an inflammatory soup (IS) to study sensitization. Urinary bladder mechanosensitive afferents were also tested. We found that baseline responses of stretch-sensitive colorectal afferents did not differ between treatment groups. Whereas IS excited a proportion of colorectal afferents CYP treatment did not alter the magnitude of this response. However, the number of stretch-sensitive fibers excited by IS was increased relative to saline-treated mice. Responses to IS were not altered by CYP treatment, but the proportion of IS-responsive fibers was increased relative to saline-treated mice. In bladder, IS application increased responses of muscular afferents to stretch, although no differences were detected between saline- and CYP-treated mice. In contrast, their chemosensitivity to IS was decreased in the CYP-treated group. Histological examination revealed no changes in colorectum and modest edema and infiltration in the urinary bladder of CYP-treated mice. In conclusion, CYP treatment increased mechanical sensitivity of colorectal muscular afferents and increased the proportion of chemosensitive colorectal afferents. These data support a peripheral contribution to cross-organ sensitization of pelvic organs. [ABSTRACT FROM AUTHOR]

Introduction: The colon and rectum are regulated by the autonomic nervous system (ANS). Abnormalities of the ANS are associated with diseases of the colon and rectum while its modulation is a putative mechanism for sacral nerve stimulation. The purpose of this study is to establish a rat model elucidating the role of the efferent ANS on rectal motility.Materials and Methods: Rectal motility following transection or stimulation of parasympathetic pelvic nerves (PN) or sympathetic hypogastric nerves (HGN) was measured with rectal strain gauge transducers and quantified as a motility index (MI). Colonic transit was measured 24 hours after transection by calculating the geometric center (GC) of distribution of (51)CrResults and Discussion: Transection of PN and HGN decreased MI to 518 +/- 185 g*s (p < 0.05) and increased MI to 5,029 +/- 1,954 g*s (p < 0.05), respectively, compared to sham (975 +/- 243 g*s). Sectioning of PN and HGN decreased transit with GC = 4.9 +/- 0.2 (p < 0.05) and increased transit with GC = 8.1 +/- 0.7 (p < 0.02), respectively, compared to sham (GC = 5.8 +/- 0.3). Stimulation of PN and HGN increased MI to 831 +/- 157% (p < 0.01) and decreased MI to 251 +/- 24% (p < 0.05), respectively.Conclusion: Rectal motility is significantly altered by sectioning or stimulating either HGN or PN. This model may be useful in studying how sacral nerve stimulation exerts its effects and provide insight into the maladies of colonic motility. [ABSTRACT FROM AUTHOR]

Pelvic nerve stimulation evokes a complex motility response in the pig rectum with a proximal decrease and a distal increase in cross-sectional area. This study investigated whether the distal increase in the cross-sectional area is because of smooth muscle relaxation mediated by nitric oxide. The pelvic nerves were stimulated with cuff electrodes in ten chloralose-anesthetized minipigs. Pressure, volume, and cross-sectional areas at five positions in the rectum were obtained during stimulation to examine the effect of NG-nitro-L-arginine (an inhibitor of nitric oxide synthase) injection. Stimulation evoked a median pressure decrease of 13 cm H2O (range, 0–27; P < 0.05; n = 10) in the anal canal, a pressure increase of 6 cm H2O (range,-15 to 30; P < 0.05; n = 10) in the rectum and a decrease of 39 mL (range, 30–63; P < 0.05; n = 6) in rectal volume. Rectal cross-sectional areas decreased 33 percent (range, 5–56; P < 0.02; n = 7) in the proximal part and increased 32 percent (range, 9–67; P < 0.02; n = 8) in the distal part. NG-nitro-L-arginine eliminated the increase in the distal rectal cross-sectional area (n = 5) and the decrease in anal canal pressure (n = 9) in all tested animals. Pelvic nerve stimulation evokes distal rectal relaxation in pigs, sensitive to NG-nitro-L-arginine, which suggests that this smooth muscle response is mediated by nitric oxide. [ABSTRACT FROM AUTHOR]

Glucose-sensitive neurons in the lateral hypothalamic area produce orexin-A (OxA) as well as orexin-B (OxB) and send their axons to the spinal dorsal horn, which predominantly expresses orexin receptor-1 (OX-1), showing a higher sensitivity to OxA. The purpose of the present study was to assess the effects of OxA on the induction of a novel form of activity-dependent reflex potentiation, spinal reflex potentiation (SRP), in the pelvic-urethral reflex activity. External urethra sphincter electromyogram in response to pelvic afferent nerve test stimulation (TS; 1/30 Hz) or repetitive stimulation (RS; 1 Hz) was recorded in anesthetized rats. TS evoked a baseline reflex activity, whereas RS produced SRP, which was abolished by intrathecal OxA (30 nM, 10 μl). tntrathecal SB- 408124 (10 μM, 10 μl), an OX-1 antagonist, reversed the abolition on SRP caused by OxA. Although there is, so far, no NR2A- and NR2B-specific agonist available, N-methyl-o-aspartate (NMDA) reversed the abolition on the RS-induced SRP caused by the co-administration of OxA and Co-101244 (30 nM, 10 μl; an NMDA NR2B subunit antagonist), but it did not reverse the abolition by the co-administration of OxA and PPPA (300 nM, 10 μl; an NMDA NR2A subunit antagonist). In conclusion, the activation of descending orexinergic fibers may inhibit the repetitive afferent input-induced central sensitization of pelvic-urethral reflex activity and urethra hyperactivity, indicating that spinal orexinergic neural transmission may be a novel target for the treatment of patients with neuropathetic or postinflammatory pain of pelvic origin. [ABSTRACT FROM AUTHOR]

Rats with experimental colitis suffer from impaired gastric emptying (GE). We previously showed that this phenomenon involves afferent neurons within the pelvic nerve. In this study, we aimed to identify the mediators involved in this afferent hyperactivation. Colitis was induced by trinitrobenzene sulfate (TNBS) instillation. We determined GE, distal front, and geometric center (GC) of intestinal transit 30 min after intragastric administration of a semiliquid Evans blue solution. We evaluated the effects of the transient receptor potential vanilloid type 1 (TRPV1) antagonists capsazepine (5–10 mg/kg) and N-(4-tertiarybutylphenyl)-4-(3-cholorphyridin-2-yl)tetrahydropyrazine-1(2H)carboxamide (BCTC; 1–10 mg/kg) and the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37) (150 μg/kg). To determine TRPV1 receptor antagonist sensitivity, we examined their effect on capsaicin-induced relaxations of isolated gastric fundus muscle strips. Immunocytochemical staining of TRPV1 and RT-PCR analysis of TRPV1 mRNA were performed in dorsal root ganglion (DRG) L6-S1. TNBS-induced colitis reduced GE but had no effect on intestinal motility. Capsazepine reduced GE in controls but had no effect in rats with colitis. At doses that had no effects in controls, BCTC and CGRP-(8–37) significantly improved colitis-induced gastroparesis. Capsazepine inhibited capsaicin-induced relaxations by 35% whereas BCTC completely abolished them. TNBS-induced colitis increased TRPV1-like immunoreactivity and TRPV1 mRNA content in pelvic afferent neuronal cell bodies in DRG L6-S1. In conclusion, distal colitis in rats impairs GE via sensitized pelvic afferent neurons. We provided pharmacological, immunocytochemical, and molecular biological evidence that this sensitization is mediated by TRPV1 receptors and involves CGRP release. [ABSTRACT FROM AUTHOR]

The current study investigates whether the spinal pelvic nerve-to-external urethra sphincter (EUS) reflex potentiation can be induced by a mechanical stimulation and whether the glutamatergic mechanism is involved in yielding such a reflex potentiation. The external urethra sphincter electromyogram (EUSE) activity, evoked by a single or by repetitive pelvic nerve stimulation, in 30 anesthetized rats was recorded with/without bladder saline distension. Without saline distension (0 cmH2O), a single pulse nerve stimulation evoked a single action potential in the reflex activity, whereas repetitive pelvic stimulation and saline distension (6-20 cmH2O) both elicited a long-lasting reflex potentiation (20.05 ± 3.21 and 75.01 ± 9.87 spikes/stimulation, respectively). The saline distension-induced pelvic nerve- to-EUS reflex potentiation was abolished by D-2-amino-5-phosphonovalerate [APV; a glutamatergic N -methyl-D-aspartic acid (NMDA) receptor antagonist; 100 µM. 10 pA, 1.72 ± 0.31 spikes/stimulation] and attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo (F) quinoxaline [NBQX; a glutamatergic α-amino-3-hydroxy- 5-methyl-4-isoxazoleproprionate (AMPA) receptor antagonist; 100 µM, 10 µl 26.16 ± 7.27 spikes/stimulation], but was not affected by bicuculline (a GABAergic antagonist; 100 µM, 10 µl, 53.62 ± 15.54 spikes/stimulation). Intrathecal administration of glutamate (31.12 ± 8.25 spikes/stimulation, 100 µM, 10 µl) and NMDA (26.25 ± 4.12 spikes/stimulation, 100 µM, 10 µl) both induced a long-lasting pelvic nerve-to-EUS reflex potentiation without saline distension, which was similar to the findings observed from saline distension only. The duration of the contraction wave of the urethra was elongated by the saline distension-induced pelvic nerve-to-EUS reflex potentiation, whereas the peak pressure of the contraction wave was not affected. Our findings suggest that saline distension in the bladder elicits a pelvic nerve-to-EUS reflex potentiation and the glutamatergic mechanism contributes to the presence of such a reflex potentiation. [ABSTRACT FROM AUTHOR]

Lower urinary tract function is regulated by spinal and supraspinal reflexes that coordinate the activity of the urinary bladder and external urethral sphincter (EUS). Two types of EUS activity (tonic and bursting) have been identified in rats. This study in urethane-anesthetized female rats used cystometry, EUS electromyography, spinal cord transection (SCT) at different segmental levels, and analysis of the effects of 5-HTIA receptor agonist (8-OH-DPAT) and antagonist (WAY 100635) drugs to examine the origin of tonic and bursting EUS activity. EUS activity was elicited by bladder distension or electrical stimulation of afferent axons in the pelvic nerve (pelvic-EUS reflex). Tonic activity evoked by bladder distension was detected in spinal cord-intact rats and after acute and chronic T8-9 or L3-4 SCT but was abolished after L6-S1 SCT. Bursting activity was abolished by all types of SCT except chronic T8-9 transection. 8-OH-DPAT enhanced tonic activity, and WAY 100635 reversed the effect of 8-OH-DPAT. The pelvic-EUS reflex consisted of an early response (ER) and late response (LR) when the bladder was distended in spinal cord-intact rats. ER remained after acute or chronic T8-9 and L3-4 SCT, but was absent after L6-S1 SCT. LR occurred only in chronic T8-9 SCT rats where it was enhanced or unmasked by 8-OH-DPAT. The results indicate that spinal serotonergic mechanisms facilitate tonic and bursting EUS activity. The circuitry for generating different patterns of EUS activity appears to be located in different segments of the spinal cord: tonic activity at L6-S1 and bursting activity between T8-9 and L3-4. [ABSTRACT FROM AUTHOR]

This study was conducted to examine reflex mechanisms that mediate urinary bladder and external urethral sphincter (EUS) coordination in urethane-anesthetized female Sprague-Dawley rats. We investigated the properties of EUS reflexes elicited by electrical stimulation of pelvic nerve afferent axons (pelvic-EUS reflex). The changes in the reflexes induced by bladder distension and administration of agonists or antagonists for glutamatergic or serotonergic receptors were examined. The reflexes consisted of an early response (ER, 18- to 22-ms latency) and a late, long-duration (>100-ms latency) response (LR), which consisted of bursts of activity at 20- to 160-ms interburst intervals. In a few experiments, a reflex with an intermediate (40- to 70-ms) latency was also identified. With the bladder empty, the ER, but not the LR, was detected in the majority of experiments. The LR was markedly enhanced when the bladder was distended. The ER remained, but the LR was abolished, after spinal cord transection at T8–T9. The ER and LR were significantly decreased 75 and 35%, respectively, by the N-methyl-ᴅ-aspartate receptor antagonist MK-801 (0.3 mg/kg iv), but only decreased 18 and 14%, respectively, by the α-amino-5-methylisoxazole-4-propionate receptor antagonist LY-215490 (3 mg/kg iv). The serotonin (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (1 mg/kg iv) enhanced spontaneous EUS activity and the pelvic-EUS reflex. WAY-100635 (0.1–1 mg/kg iv), a 5-HT1A antagonist, reversed the effect of 8-hydroxy-2-(di-n-propylamino)-tetralin and suppressed EUS activity and the pelvic-EUS reflex. These results indicate that glutamatergic and serotonergic mechanisms are important in the reflex pathways underlying bladder-sphincter coordination in rats. [ABSTRACT FROM AUTHOR]

Acupuncture is useful for functional bowel diseases, such as constipation and diarrhea. However, the mechanisms of beneficial effects of acupuncture on colonic function have scarcely ever been investigated. We tested the hypothesis that electroacupuncture (EA) at ST-36 stimulates colonic motility and transit via a parasympathetic pathway in conscious rats. Hook-shaped needles were inserted at bilateral ST-36 (lower limb) or BL-21 (back) and electrically stimulated at 10 Hz for 20 mm. We also studied c-Fos expression in response to EA at ST-36 in Barrington's nucleus of the pons. EA at ST-36, but not BL-21, significantly increased the amplitude of motility at the distal colon. The calculated motility index of the distal colon increased to 132 ± 9.9% of basal levels (n = 14, P < 0.05). In contrast, EA at ST-36 had no stimulatory effects in the proximal colon. EA at ST-36 significantly accelerated colonic transit [geometric center (GC) = 6.76 ± 0.42, n = 9, P < 0.001] compared with EA at BL-21 (GC = 5.23 ± 0.39, n = 7). The stimulatory effect of EA at ST-36 on colonic motility and transit was abolished by pretreatment with atropine. EA-induced acceleration of colonic transit was also abolished by extrinsic nerve denervation of the distal colon (GC = 4.69 ± 0.33, n = 6). The number of c-Fos-immunopositive cells at Barrington's nucleus significantly increased in response to EA at ST-36 to 8.1 ± 1.1 cells/section compared with that of controls (2.4 ± 0.5 cells/section, n = 3, P < 0.01). It is concluded that EA at ST-36 stimulates distal colonic motility and accelerates colonic transit via a sacral parasympathetic efferent pathway (pelvic nerve). Barrington's nucleus plays an important role in mediating EA-induced distal colonic motility in conscious rats. [ABSTRACT FROM AUTHOR]

The aim of the present study is to symptomatically analyze the extent to which pelvic nerve-sparing radical surgery for rectal cancer impacts on long-term voiding and male sexual function.A self-administered questionnaire was mailed to 68 patients who underwent pelvic nerve-sparing radical surgery for invasive rectal cancer with 52 responses (28 men and 24 women; 27 complete and 25 incomplete preservation; response rate 76.5%). Each patient was asked to record if there had been any changes in lower urinary tract symptoms after surgery. Sexual function was also investigated in men.Of the 52 patients, 48 (92%) maintained voluntary voiding without catheterization in the long term. Clean intermittent self-catheterization was performed in only four patients with incomplete preservation because of persistent voiding dysfunction. Subjectively, approximately 60% of the patients remained unchanged in lower urinary tract symptoms after surgery. The satisfaction rate regarding the current voiding status was significantly higher in women than in men (83% versus 61%,P = 0.0294), but was not significantly different between those with complete (76%) and incomplete preservation (64%). Despite the acceptable urinary status, 88% of men had some deterioration in the erectile function, regardless of the types of surgical procedures. Overall, 64% of men were unsatisfied with the current sexual function.Pelvic nerve-sparing radical surgery for rectal cancer preserved the long-term voiding function in the majority of patients. In completely preserved patients and in women, symptomatic outcomes were more satisfactory. Postoperative erectile dysfunction was found to be a serious problem, even in complete nerve-sparing procedure. [ABSTRACT FROM AUTHOR]

Reflex plasticity between pelvic afferent and pudendal efferent nerve fibers was examined in anesthetized rats. Brief high-frequency electric stimulation (300 pulses at 100 Hz) of the pelvic nerve afferent fiber produced a long-lasting potentiation of the pelvic-to-pudendal reflex (PPR). This tetanization-induced potentiation was abolished by a selective Nmethyl-D-aspartate (NMDA) receptor antagonist and attenuated by a non-NMDA excitatory amino acid receptor antagonist. However, the GABAA-receptor antagonist had no effect on this potentiation. Both intrathecal glutamate (0.1 mM, 2-5 µl it) and NMDA (0.1 mM, 2-5 µl it) induced a potentiation of PPR similar to that of tetanization. Agonist-induced potentiation was shorter than tetanization-induced potentiation. The duration of the contraction wave of intraurethral pressure, elicited by PPR, was elongated by tetanization-induced potentiation, whereas the peak pressure was not affected. All these results demonstrate that brief high-frequency stimulation of the pelvic nerve afferent fiber can induce a distinct and long-lasting modulation in PPR activity and this change may be involved in nociceptive C afferent-induced obstructive urinary dysfunctions. [ABSTRACT FROM AUTHOR]

The discharge characteristics of sacral visceral afferents supplying the urinary bladder, urethra, colon and anus to mechanical stimuli were analyzed in the anaesthetized cat. The stimuli used were passive distension (urinary bladder, colon), isovolumetric contraction (urinary bladder), movements of the urethral catheter and mechanical shearing stimuli (mucosal skin of the anal canal). (1) In total 245 afferent units which projected in the pelvic nerve were isolated from the sacral dorsal roots. From one of the following organs, urinary bladder, colon, urethra and anus 117 afferent units were activated. By these stimuli from the bladder, urethra and anus 122 afferent units could not be activated, and as far as tested also not from the colon; in 6 afferent units the classification was unclear. (2) Afferent units from the urinary bladder and the colon responded consistently to passive distension of the respective organ. The units from the urinary bladder showed graded responses at intraluminal pressures of about 10-70 mm Hg and responded also to isovolumetric contractions of the organ. The thresholds of the units from the bladder to passive distension and contraction varied from about 5 to 20 mm Hg intravesical pressure. (3) The afferent units from the urethra and the anus did not react or showed some weak phasic and irregular responses to distension and contraction applied to the urinary bladder or to distension of the colon. They were consistently excited by low threshold mechanical stimulation of the urethra and anus, respectively. (4) The axons from the bladder, urethra and anus were presumably myelinated (conduction velocity above 2 m/s) and conducted at 10.3±6.1 m/s ( n=34, mean±SD), 26.3±9.3 m/s ( n=13) and 9.5±5.1 m/s ( n=37), respectively. The axons from the colon conducted at about 0.5 to 16 m/s ( n=20), 13 of them conducting at less than 2 m/s. About 75% of the axons which could not be activated by mechanical stimulation of the visceral organs were presumably unmyelinated (conduction velocity below 2 m/s). (5) Some ongoing activity was found in 9 out of 26 afferent units from the anus but, with one exception, the afferent units from the bladder, urethra and colon were silent. (6) It is concluded that the pelvic afferent units from the urinary bladder, urethra, colon and anus consist of distinct populations with characteristic response patterns. There is no indication from this investigation that the urinary bladder is supplied by sacral afferents which are only recruited at high intravesical pressures during passive distension and isovolumetric contractions and which are possibly associated with pain. [ABSTRACT FROM AUTHOR]

Inhibition of the micturition, defecation and rhythmic straining reflexes by midbrain stimulation was compared with the inhibition of the jaw-opening reflex caused by tooth pulp stimulation in decerebrate dogs. All of the reflexes were inhibited by stimulation of the dorsal and ventral periaqueductal gray, dorsal raphe nucleus and central tegmental field with similar threshold intensities. After a hemisection of the spinal cord at the C2 segment, the midbrain stimulation still suppressed the micturition reflex as well as field potential changes which were evoked by stimulation of the pelvic nerve and recorded from the lateral funiculus just caudal to the hemisection, but did not influence the discharges of the vesical branch of the pelvic nerve which were elicited by stimulation of the lateral funiculus just rostral to the hemisection. The results suggest that stimulation of the neural elements in the 4 midbrain areas depresses the ascending activities from vesical and colorectal afferents of the pelvic nerve at the spinal level, and consequently inhibits the pelvic nerve reflexes. Systemic methysergide suppressed midbrain inhibition of the jaw-opening reflex, but did not affect the midbrain inhibition of the pelvic nerve reflexes. Systemic naloxone did not influence midbrain inhibition of the pelvic nerve reflexes or the jaw-opening reflex, but enhanced the micturition and rhythmic straining reflexes. Possible roles of the midbrain inhibition of the pelvic nerve reflexes are discussed. [ABSTRACT FROM AUTHOR]

Supraspinal descending influences on the sacral parasympathetic outflow were tested recording spontaneous and reflex activity of the pelvic nerves in cats. Peripheral chemoreceptor activation enhanced the spontaneous discharge of pelvic efferents. Baroreceptor activation reduced the spontaneous activity as well as the late components of viscero- and somato-visceral reflexes. Acute spinalization (C) abolished the late reflex components. It enhanced the spontaneous activity and sometimes induced rhythmic discharges of the pelvic efferents. Simultaneous recording of lumbar white ramus and pelvic nerve activity suggests that the tested descending influences may act on the sacral parasympathetic preganglionic nervous activity and on the lumbar sympathetic preganglionic activity in a similar manner. [ABSTRACT FROM AUTHOR]

Bilateral section of either the sensory or motor branch of the pelvic nerve or pudendal nerve was performed in rats on days 8-10 of pregnancy, and the effects on delivery were observed. Bilateral resection of the sensory branch of the pelvic nerve reduced the number of live pups per litter, and increased the number of stillbirths and the number of fetuses retained in utero per litter at day 24. Sectioning motor components of the pelvic nerve, or both motor and sensory components of the pudendal nerve, had no effects on delivery in rats. We conclude that of the peripheral nerves evaluated in this study, only the sensory branch of the pelvic nerve is required for normal vaginal delivery in this species. [ABSTRACT FROM AUTHOR]