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The hypogastric nerves take an arterial supply from the internal iliac artery either directly or from one of its main branches close to its origin from the parent trunk. Sometimes the supply is from the lower end of the common iliac artery. In half the cases examined the presacral nerve takes an arterial supply from the aorta at its bifurcation.
This paper presents a study of urethral responses to efferent nerve stimulation in dogs. The pelvic, hypogastric and pudendal nerves were stimulated using a programmed instrument under three different in vivo conditions. The preparations consisted of: (A) bladder, urethra, and rectum; (B) urethra and rectum, and (C) urethra only. Stimulation of the pelvic nerve in preparation A resulted in elongation and constriction of the mid and proximal urethra with a resultant rise in pressure. However, this response was reduced in preparations B and C. Similar observations were made with hypogastric nerve stimulation. The results of pudendal nerve stimulation were significantly different, in that the pressure rise occurred in the mild and distal urethra and varied in elongation response.
The functional activity of the sphincter muscle of the urethra is known to be controlled largely by the hypogastric and pudendal nerves. It remains unknown, however, whether innervation of the muscle by these peripheral nerves is ipsi- or bilateral. In an attempt to answer this question urethral closure pressure was determined simultaneously in the anterior, posterior, right and left portions of urethral wall in dogs. The pressure measurements were stereographed with the aid of a computer (stereo-UPP) and by this means the effect of unilateral section or electrical stimulation of hypogastric and pudendal nerves on the intraurethral pressure profile was analyzed. Unilateral section or electrical stimulation of the hypogastric nerve, distal to its division, produced a fall and a rise primarily in proximal intraurethral pressure, respectively, in all four directions. There was no significant difference in this response between the involved and uninvolved sides. Unilateral section of the pudendal nerve resulted in a fall primarily in distal intraurethral pressure in all four directions. No significant difference was present between the injured and noninjured sides. In contrast, electrical stimulation of the pudendal nerve distal to the point of its division caused a rise in intraurethral pressure in all four directions, with a significantly greater pressor response on the stimulated than on the nonstimulated side. These observations suggest decussating motor innervation of the urethra by the hypogastric nerves and also the possibility of the distal urethra being ipsilaterally innervated by the pudendal nerve.
The effects of electrical stimulation of hypogastric nerve and sympathetic chain on 'electroerection' (penile erection induced by electrical stimulation of the pelvic nerve) were studied in dogs to clarify the physiological roles that these neural inputs may play in producing and/or maintaining penile erection. As an objective parameter of hemodynamics of the penile circulation, the pressure in the corpus cavernosum of the penis was measured. Hypogastric nerve electrostimulation was performed in 24 dogs who had received pelvic nerve stimulation and, therefore, had 'electroerection'. Ten dogs responded to this procedure with an augmentation of 'electroerection', 10 with an attenuation of 'electroerection', and 4 with no appreciable changes. 4 out of the 10 animals who exhibited an attenuation response were then given an alpha 1-adrenergic blocker (prazosin hydrochloride) prior to the electrical stimulation to evaluate the specificity of the effects of the hypogastric nerve stimulation. In 3 of the 4 dogs the attenuation effect was abolished by this treatment and instead an augmentation effect became evident. Sympathetic chain electrostimulation was performed in 6 dogs with 'electroerection'. When applied to the L4-5 interganglionic segment, it produced a biphasic response which consisted of an initial increase followed by a decrease of the intracorporeal pressure. In contrast, stimulation of the L2-3 interganglionic segment produced a monophasic response consisting of only augmentation of the intracorporeal pressure. These data suggested that there might be two groups of fibers in the hypogastric nerve and sympathetic chain which are functioning antagonistically, and that the anti-erectile neural inputs are mediated primarily by the alpha 1-adrenergic system. To examine the sites of penile vasculature where the innervating hypogastric nerve exerts its effects, electrical pelvic/hypogastric nerve stimulations were performed in dogs in whom the inflow blood circulation to the corpora cavernosa was disrupted by arterial ligation and replaced by a constant saline infusion. It appears that the stimulatory input via the hypogastric nerve caused an increased blood flow into the cavernous space due to vasodilation of the inflow blood vessels, and the inhibitory effect occurred mainly due to relaxation of the draining blood vessels with a resultant increase of the blood outflow from the cavernous space.
Considerable evidence has accumulated in recent years to suggest that cyclic AMP-dependent protein kinase is responsible for the activation of tyrosine hydroxylase following nerve stimulation. Since stimulation of the central nervous system either by electrical impulses or by exposure of intact brain tissue to depolarizing concentrations of potassium is associated with an activation of adenylate cyclase and an increase in cyclic AMP, it is possible that the normal physiological mechanism by which catecholamine synthesis is enhanced during nerve stimulation involves modification of the enzyme by protein kinase. It has been demonstrated that, in the presence of cyclic AMP, ATP, Mg++ and protein kinase, purified preparations of tyrosine hydroxylase are directly phosphorylated. Since cyclic nucleotides also have been implicated in the process of neurally mediated transmitter release, it is conceivable that activation of adenylate cyclase presynaptically is a common mechanism by which both catecholamine synthesis and norepinephrine release are enhanced during nerve stimulation. Although agonists and antagonists of many putative presynaptic receptors have been found to modulate norepinephrine release during nerve stimulation, no convincing evidence has yet been obtained to suggest that alteration of presynaptic adenylate cyclase activity consequent to nerve stimulation is mediated by a presynaptic action of one or more of these neuromodulators. It is possible that direct depolarization of the nerve terminal in some manner results in activation of presynaptic adenylate cyclase, perhaps by a mechanism involving calcium.
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The retrospective study of 38 male patients undergoing aorto-iliac reconstructive and abdominal aortic aneurysm surgery was carried out. The study demonstrates the deficiency in the pre-operative, intra-operative, and post-operative evaluation of these patients regarding the factors affecting impotence. Recommendations are made, and a flow sheet is compiled to assist the vascular surgeon in the evaluation and management of these patients.
The hypogastric nerve (HGN) is a sympathetic nerve in the peritoneal cavity and controls urinary and seminal functions. In this study, the regeneration of HGN was determined by using a new type of an artificial nerve conduit, polyglycolic acid (PGA)-collagen nerve conduit filled with collagen sponge in two dogs. A PGA-collagen nerve conduit (diameter=2 mm) was interposed in a 10 mm gap of the right HGN. The regeneration of the HGN was evaluated electrophysiologically 8 months after the operation. The intraluminal pressure of spermatic duct and the bladder neck were elevated 80 mmHg and 25 mmHg respectively by the stimulation across the regenerated HGN. The prostate contraction was also elicited. The responses diminished after the excision of the regenerated portion of HGN. These results proved the regeneration of HGN and this nerve conduit will be great help for patients who suffer from urinary and seminal disturbances.
Whole-nerve cuff electrodes can be used to record electrical nerve activity in peripheral nerves and are suitable for chronic implantation in animals or humans. If the whole nerve innervates multiple target organs or muscles then the recorded activity will be the superposition of the activity of different nerve fibers innervating these organs. In certain cases it is desirable to monitor mixed nerve activity and to determine the origin (modality) of the recorded activity. A method using the autocorrelation function of recorded nerve activity and an artificial neural network was developed to classify the modality of nerve signals. The method works in cases where different end organs are innervated by nerve fibers having different diameter distributions. The electrical activity in the cat S1 sacral spinal root was recorded using a cuff electrode during the activation of cutaneous, bladder, and rectal mechanoreceptors. Using the classification method, 87.5% of nerve signals were correctly classified. This result demonstrates the effectiveness of the neural network classification method to determine the modality of the nerve activity arising from activation of different receptors.
Electrical stimulation of peripheral nerves can be used to cause muscle contraction, to activate reflexes, and to modulate some functions of the central nervous system (neuromodulation). If applied to the spinal cord or nerves controlling the lower urinary tract, electrical stimulation can produce bladder or sphincter contraction, produce micturition, and can be applied as a medical treatment in cases of incontinence and urinary retention. This article first reviews the history of electrical stimulation applied for treatment of bladder dysfunction and then focuses on the implantable Finetech-Brindley stimulator to produce bladder emptying, and on external and implantable neuromodulation systems for treatment of incontinence. We conclude by summarizing some recent research efforts including: (a) combined sacral posterior and anterior sacral root stimulator implant (SPARSI), (b) selective stimulation of nerve fibers for selective detrusor activation by sacral ventral root stimulation, (c) microstimulation of the spinal cord, and (d) a newly proposed closed-loop bladder neuroprosthesis to treat incontinence caused by bladder overactivity.
Expression and androgen regulation of the gene for neuronal nitric oxide synthase (NOS I) were examined in neurons of the major pelvic ganglia in male rats. Some of these postganglionic neurons innervate the penis and produce nitric oxide, which is believed to play a major role in penile erection. Rats were either castrated or sham operated and implanted with SILASTIC brand capsules filled with powdered testosterone (T) or 5alpha-dihydrotestosterone (5alphaDHT) or left empty. After 4 days, the number of neurons intensely stained for NADPH-diaphorase as well as those giving a NOS I signal in in situ hybridization experiments increased in castrated rats treated with testosterone by 31% and 42%, respectively, relative to those in untreated castrated rats. This suggests that the increase in NADPH-diaphorase activity resulted from enzyme synthesis and was due to a modification of NOS I messenger RNA (mRNA) accumulation. After 7 days, Northern blot analysis showed that castration produced a decrease in the amount of NOS I mRNA relative to that of ribosomal RNA. This decrease was almost prevented by T treatment. No significant differences were observed by reverse transcriptase-PCR between 7-day and 28-day treatments. However, in 7-day castrated rats treated with 5alphaDHT, NOS I signals relative to those of hypoxanthine phosphoribosyltransferase, taken as reference, were significantly higher than those in castrated rats and resembled those in sham-castrated rats, suggesting that 5alphaDHT was probably more potent than testosterone in preventing the decrease in NOS I mRNA levels elicited by castration. These results show that NOS I can be positively regulated by androgens and are consistent with the suggestion that these steroids play a role in the physiological processes of penile erection.
Erectile dysfunction is commonly experienced in men with diabetes mellitus. We report that the intracavernous pressure (ICP) rise in diabetic rats was 55% of the control and returned to normal following insulin (I) or insulin plus free oxygen scavenger (I + S) treatment. Insulin-like growth factor (IGF) binding protein (IGFBP) -3, -4, and -5 messenger RNA (mRNA) levels in the major pelvic ganglia (MPG) of diabetic rats were elevated by 2-fold, 2.6-fold, and 2.5-fold, respectively. Both I and I + S returned IGFBP-4 and 5 mRNA levels to normal, whereas IGFBP-3 gene expression was severely inhibited. IGFBP-2 gene expression was greatly inhibited by diabetes and was unresponsive to treatment. In the penis of diabetic rats, IGFBP-2 and -4 mRNA levels were low, whereas IGFBP-3 mRNA levels were elevated 10-fold. These effects were reversed by I and I + S. I and I + S also corrected the IGFBP-3 expression pattern. IGF-I gene expression in the penis and MPG was not significantly increased (P < 0.05) by diabetes and returned to normal levels following I or I + S treatment. Because IGFs are potent regulatory factors in vascular tone, this newly described activity of insulin may play an important role in the improvement of erectile function seen clinically and in animal models.
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The study of mammalian neural crest development has been limited by the lack of an accessible system for in vivo transplantation of these cells. We have developed a novel transplantation system to study lineage restriction in the rodent neural crest. Migratory rat neural crest cells (NCCs), transplanted into chicken embryos, can differentiate into sensory, sympathetic, and parasympathetic neurons, as shown by the expression of neuronal subtype-specific and pan-neuronal markers, as well as into Schwann cells and satellite glia. In contrast, an immunopurified population of enteric neural precursors (ENPs) from the fetal gut can also generate neurons in all of these ganglia, but only expresses appropriate neuronal subtype markers in Remak's and associated pelvic parasympathetic ganglia. ENPs also appear restricted in the kinds of glia they can generate in comparison to NCCs. Thus ENPs have parasympathetic and presumably enteric capacities, but not sympathetic or sensory capacities. These results identify a new autonomic lineage restriction in the neural crest, and suggest that this restriction preceeds the choice between neuronal and glial fates.
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We compared the urethral and cardiovascular effects of silodosin (selective alpha(1A)-adrenoceptor antagonist), a novel medication for benign prostatic hyperplasia (BPH), with those of tamsulosin (selective alpha(1A)/alpha(1D)-adrenoceptor antagonist) and naftopidil (selective alpha(1D)-adrenoceptor antagonist). We evaluated the effects of these three drugs on the increase in intraurethral pressure (IUP) induced by electrical stimulation of the hypogastric nerve in anesthetized dogs with spontaneous BPH. All three drugs dose-dependently reduced both the increase in IUP and the mean blood pressure (MBP). The rank order of potencies was tamsulosin>silodosin>naftopidil for the reductions in both IUP and MBP. However, the uroselectivity (ED(15) value for hypotensive effect/ID(50) value for reduction in IUP) of silodosin (uroselectivity, 19.8) was about 21 and 4 times higher than that of tamsulosin (0.939) and naftopidil (4.94), respectively. These data suggest that silodosin might be one of the most useful medications for dysuria in BPH patients.
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Effects of selective applications of drugs to the guinea pig hypogastric ganglion were studied on the contractile response of the vas deferens to the hypogastric nerve stimulation or to ganglionic stimulating drugs. Both acetylcholine (ACh) and dimethylphenylpiperazinium (DMPP) contracted the vas deferens. Neostigmine potentiated the ACh-induced contractions but not those which were DMPP-induced. Hemicholinium-3 (HC-3) reduced the response to nerve stimulation (R-NS) but affected neither the ACh-induced contractions nor the DMPP-induced contractions. Morphine blocked R-NS but not the ACh-induced and the DMPP-induced contractions. Hexamethonium reduced R-NS and the contractions to ACh or to DMPP. Methacholine and bethanechol applied before and after preganglionic tetanic stimulation of the hypogastric nerve produced no change of tone of the vas deferens. Atropine did not antagonize the responses which were produced by nerve stimulation, ACh or DMPP. These results support the classic hypothesis that ganglionic transmission is mediated by nicotinic receptors but do not provide evidence that muscarinic receptors exist at the synapses of this preparation.