Seminal Emission Research Articles

Effects of the Artificial Urinary Sphincter on Prostatic Development and Sexual Function in Pubertal Boys with Meningomyelocele

Although sexual development in boys with meningiomyelocele may progress normally through puberty, the effects of surgical correction of incontinence by insertion of an artificial sphincter device around the bladder neck remain unclear. We studied 13 boys who received an artificial urinary sphincter before puberty and compared them to 12 age-matched pubertal controls with meningomyelocele. The prostate morphology was evaluated by means of transrectal ultrasonography, and we compared this finding, as well as sexual development, erectile function and seminal emissions between the 2 groups.Boys in both groups had similar development of secondary sexual characteristics and reported similar erectile function. Ultrasonography demonstrated an imprint of the sphincter cuff on the prostate but patients and controls had equal prostatic growth. In both groups an unexpected finding was the unexplained presence of sonolucent and sonodense lesions within the prostate glands.We conclude that transrectal ultrasonography is an excellent means of examining the prostate in pubertal boys with meningomyelocele. An artificial urinary sphincter placed around the bladder neck does not alter sexual development, function, prostatic growth or prostatic morphology.

Electroejaculation in Spinal Cord Injury Patients: Simplified New Equipment and Technique

A new simplified electrostimulation system for rectal probe electroejaculation has been developed and tested 17 times in 13 patients. Seminal emissions were obtained easily from 13 of 17 studies and partial emissions were obtained in 4. Patients with cauda equina and conus lesions with partial intact sensorium also could achieve successful ejaculation by longer stimulation from 2 to 5minutes with lower currents that could be maintained easily and were tolerated by the patient—a feature unique to our new computerized equipment. The simplicity of operation reduces the number of trained personnel for an electrostimulation procedure, which can be done even in an outpatient setting. (J. Urol., 143: 305–307, 1990).

Clonidine Suppresses Copulatory Behavior and Erectile Reflexes in Male Rats: Lack of Effect of Naloxone Pretreatment

Adrenergic transmitters and opioid peptides are implicated in the regulation of male sexual behavior. In the present studies we examine a possible interaction between these two neurochemical systems in the regulation of components of male sexual behavior. In mating tests, clonidine (0.25 mg/kg, 6 min pretest) induced a profound deficit in intromissive and ejaculatory behavior whereas naloxone (5 mg/kg, 20 min pretest) evinced a facilitation of ejaculatory behavior, evidenced by decreases in the ejaculation latency in the initial copulatory series and by decreases in ejaculation latency and intercopulatory interval in the second copulatory series. Importantly, prior treatment with naloxone did not prevent or attenuate the copulatory suppression induced by clonidine. In ex copula penile reflex tests, clonidine (0.25 mg/kg, 6 min pretest) decreased the incidence of seminal emission and the number of penile responses (erections, cups and flips). Naloxone (5 mg/kg, 20 min pretest) was without effect on any of the parameters of penile reflex activity and, further, failed to prevent or attenuate the erectile suppression induced by clonidine. A final study evaluated the dose-response relationship of clonidine-induced erectile dysfunction. A similar degree of erectile dysfunction was observed after 0.005, 0.025 or 0.25 mg/kg clonidine, whereas 0.0005 mg/kg was without effect. Previous studies demonstrated a dose-dependent inhibition of mounting, intromissive and ejaculatory behavior, with 0.25 mg/kg selectively eliminating ejaculatory behavior in mating tests. These data demonstrate a dose-dependent inhibition of penile reflexes, with inhibition occurring at doses lower than those required to induce copulatory dysfunction. Further, we suggest that opioid receptors sensitive to naloxone blockade are not involved in the clonidine-induced suppression of copulatory or erectile function.

An experimental examination of the colour component in visually mediated sexual arousal of the male chacma baboon (Papio ursinus)

Male chacma baboon (Papio ursinus) sexual arousal response as gauged by the coagulated seminal emissions resultant from masturbatory activity was experimentally assessed. Males were initially exposed to an ovariectomized female prior to and during daily oestradiol benzoate treatment. Males were then re‐exposed to the same female prior to and during the wearing of a thermoplastic model of a swollen female perineum. A total of eight different colours were sequentially applied to the model. It was only the red model that elicited a response similar to that shown to the oestradiol‐treated female. The behavioural data collected from the stimulus female supported the view that it was model colour that determined the differential male response.

Quinelorane (LY163502), a D2 dopamine receptor agonist, facilitatesseminal emission, but inhibits penile erection in the rat

Dopaminergic compounds have been shown to facilitate male sexual responses in various contexts. We investigated the effects of a specific D2 dopamine receptor agonist, quinelorane (LY163502), on sexual responses elicited in the restrained supine male rat (i.e., ex copula reflex tests). Penile erections, evoked by retraction of the penile sheath, were inhibited by systemic administration of 10 micrograms/kg quinelorane; however, the occurrence of seminal emission was dramatically increased. A smaller dose of 0.25 ng/kg was without effect. In a second experiment, intracranial microinjection of quinelorane was followed by ex copula reflex tests. The medial preoptic area (MPOA) has been previously implicated in the dopaminergic regulation of male copulatory behavior. The effects of an intra-MPOA injection of quinelorane on seminal emission and erectile responses were similar to those observed following systemic administration. These results are consistent with the hypothesis that DA receptors in the MPOA are important in the regulation of male sexual behavior and suggest that D2 receptors in the MPOA may decrease ejaculatory threshold while inhibiting erectile mechanisms.

The effects of intracranial administration of the dopamine agonist apomorphine on penile reflexes and seminal emission in the rat

Previous studies employing systemic administration of the dopamine agonist apomorphine have shown that the dose response curves for apomorphine's effects on penile reflexes and seminal emission differ, suggesting that experimentally separable populations of dopamine receptors regulate these two responses. The present experiments examined the locations of central nervous system DA receptors mediating genital responses in the restrained, supine rat by injecing apomorphine into the medial preoptic area and the paraventricular nucleus through chronic, indwelling cannulae. Medial preoptic area injections facilitated penile reflexes, but not seminal emission, while paraventricular injections facilitated seminal emission. These results suggest that systemically administered apomorphine may facilitate penile reflexes by acting on the medial preoptic area and may enhance seminal emission by acting on the paraventricular nucleus.

Hypogastric plexus stimulators for obtaining semen from paraplegic men.

Radio-linked devices to stimulate the hypogastric plexus have been implanted into 7 patients with spinal injuries and 1 with primary anorgasmia. They caused seminal emission in all patients and still do so in the spinal injury patients. Insemination with semen thus obtained has yielded 5 pregnancies (2 live births) in the wives of 4 patients. The range of application is discussed.

EFFECTS OF ATROPINE ON FERTILITY OF MALE RATS

Insertion of silastic rods containing 25% and 50% atropine adjacent to the epididymis of rats produced a significant suppression in fertility which was temporary with the lower dose and permanent with the higher dose. Both doses also impaired the motility of epididymal spermatozoa and nerve-mediated contractile response of isolated vasa deferentia. In addition, the higher dose caused a significant reduction in the mating frequency. It is concluded that the antifertility effect resulted primarily from oligospermia due to dysfunctioning of seminal emission and/or ejaculation.

The Ferrier lecture, 1986. The actions of parasympathetic and sympathetic nerves in human micturition, erection and seminal emission, and their restoration in paraplegic patients by implanted electrical stimulators.

Implants that stimulate the S2, S3 and S4 anterior roots improve micturition, defaecation and penile erection in many patients with spinal-cord injuries. The posterior rhizotomy that is commonly done at the same time usually cures their urinary incontinence, and may greatly improve bladder compliance. Implants that stimulate the hypogastric plexus allow semen to be obtained easily from some men with spinal injuries who cannot ejaculate, and may allow an implant-driven erection. A little new knowledge about the neurophysiology of the pelvic organs has come from studying the performance of these implants.

Stimulation of opioid receptors suppresses penile erectile reflexes and seminal emission in rats

The effects of several doses of morphine and naloxone, given alone or in combination, on ex copula tests for rat penile erectile responses and seminal emission were studied. Morphine (0.1, 0.5, 1 and 5 mg/kg IP, 30 min before the test) reduced the proportion of animals showing erections in a dose-related fashion. Seminal emission was apparently more sensitive to opioid inhibition than erectile responses, since it was virtually suppressed by all the doses of morphine tested. Naloxone given alone (0.1, 1 and 10 mg/kg IP, 15 min before testing) was largely ineffective on these genital responses although a significant decrease in the display of erection was observed with the lowest dose. Naloxone (1 mg/kg) efficiently antagonized the effects of morphine (1, 5 and 25 mg/kg) on erectile responses and all but the largest dose of the opiate agonist on seminal emission. These results indicate that, in addition to the well-documented effects of opioids on sexual drive, their effects on the genital reflex potential could play a major role in the sexual deficits associated to opiate intake.

Apomorphine and haloperidol, but not domperidone, affect penile reflexes in rats

Previous studies have shown that systematic administration of the dopamine agonist apomorphine produced a biphasic effect on erection in the freely moving rat, with lower doses facilitating, and high doses inhibiting, erection. However, those studies did not distinguish between erection per se and seminal emission. The present results demonstrate that apomorphine produces a similar biphasic effect on penile reflexes in the restrained, supine rat, while facilitating seminal emission in a monophasic fashion. Haloperidol, a centrally-acting dopamine antagonist, either blocked the effects produced by apomorphine administration, or had actions opposite to those of apomorphine. Domperidone, a dopamine antagonist that does not readily penetrate the blood-brain barrier, did not antagonize apomorphine's effects, and did not affect penile responses when administered alone. These results suggest that dopamine receptors in the central nervous system regulate genital responses, and that effects on penile reflexes and seminal emission can be experimentally dissociated.

Drug-Induced Male Sexual Dysfunction

Many commonly used drugs can interfere with male sexual function, either by decreasing libido, interfering with erectile function, or causing absent seminal emission or retrograde ejaculation. Although drug-related effects on sexual function may be difficult to distinguish from the effects of organic disease, anxiety, or depression, it is important for the physician to be aware of the drugs most commonly associated with sexual dysfunction. This article considers these drugs and the potential mechanism by which they exert their adverse effects.

Chlordiazepoxide facilitates erections and inhibits seminal emission in rats.

Two experiments have been conducted to clarify the effects of the benzodiazepine chlordiazepoxide (CDP) on the different components of male rat sexual behavior. In the first experiment the effects on penile erectile reflexes (PR) of two doses (10 and 30 mg/kg, IP) of CDP were compared with those of vehicle, no-treatment and baseline pre-test in a repeated measures design. In the second experiment the different components of male sexual behavior - PR, mating behavior and spontaneous seminal emission SSE) - were extensively studied after vehicle, 3 and 30 mg/kg CDP treatments. CDP was found to increase significantly the percentage of rats showing penile reflexes, enhance the number of erections per test and shorten the latency to onset of reflexes. It lowered the percentage of animals displaying seminal emission during the PR test. In the mating behavior test, CDP abolished copulatory (and other) behavior at 30 mg/kg. It decreased the number of animals achieving ejaculation at the subataxic 3 mg/kg dose level. In the SSE 3-day test, CDP significantly reduced the weight and the number of plugs of seminal material emitted by the CDP-injected animals. The possible involvement of the serotonergic system in determining the dose-dependent increase in erections and decrease in seminal emission following CDP treatments is discussed. Clinical implications are also briefly considered.

Effects of a selective alpha 1-adrenoceptor agonist, methoxamine, on sexual behavior and penile reflexes

Methoxamine, an adrenergic agonist with selectivity for the alpha 1-adrenoceptor, when administered intraperitoneally 10 minutes prior to mating tests (1 to 5 mg/kg), effected reductions in the ejaculatory threshold, evidenced by a decrease in the number of intromissions preceding ejaculation. In mounting tests after penile anesthetization, a test which specifically assesses sexual motivation, 3 mg/kg methoxamine was without a stimulatory effect. Further, in penile reflex tests ( ex copula) 1 mg/kg methoxamine was without effect, whereas 5 mg/kg decreased the number of erections, cups and flips per test, and increased the incidence of seminal emission. These data indicate a facilitation of the ejaculatory mechanism, both in and ex copula, coupled with an inhibition of erectile responses for moderate doses of methoxamine. Treatment of male rats with the alpha 2-adrenoceptor agonist clonidine (0.25 mg/kg, IP, five minutes pretest) drastically reduced the number of animals exhibiting intromissive and ejaculatory behavior in mating tests. This suppressive effect of clonidine was not prevented by prior treatment with methoxamine (3 mg/kg, 10 minutes pretest and five minutes preclonidine). Further, ST-91, a polar analog of clonidine which does not readily enter the central nervous system, was without effect on male sexual behavior. Since (1) the effects of methoxamine administration are not of similar quality or magnitude to those reported earlier after yohimbine, an alpha 2-adrenoceptor antagonist, (2) since concurrent stimulation of alpha 1- (by methoxamine) and alpha 2- (by clonidine) adrenoceptors is followed by a suppression of sexual behavior similar to that seen after clonidine alone, and (3) since a peripherally acting alpha 2-adrenoceptor agonist is without effect on sexual behavior, we suggest that one of the substrates underlying the clonidine-induced suppression of male rats' sexual behavior are postsynaptic alpha 2-adrenoceptors located within the central nervous system. Further, alpha 1-adrenoceptors appear to play a role in the regulation of the ejaculatory threshold in and ex copula, and in the regulation of erection ex copula.

Genital responses in noncopulators and rats with lesions in the medial preoptic area or midthoracic spinal cord

To determine whether genital dys-function participates in the sexual inactivity of noncopulator and MPOA-lesioned rats, penile reflexes and spontaneous seminal emission (SSE) were investigated in such animals. The display of penile reflexes was either the same or enhanced in these animals, relative to controls. Noncopulators and MPOA-lesioned rats also did not differ from controls in SSE. Plasma testosterone levels showed no differences between noncopulators and sexually active controls but tended to be elevated in rats bearing MPOA lesions. Finally, SSE did not differ between rats with midthoracic spinal cord transections and controls, suggesting that SSE is not under supraspinal inhibition.

Failure of pimozide and metergoline to antagonize the RDS-127-induced facilitation of ejaculatory behavior

Metergoline, a serotonin-receptor antagonist, when administered in either an ascorbic acid or ethanol containing vehicle was without effect on male rat copulatory behavior (3 mg/kg, 90 minutes pretest). When initially dissolved in several drops of acetic acid, however, the same dose of metergoline dramatically suppressed male rat sexual behavior. Thus, one-half of the treated rats failed to intromit and ejaculate, and those displaying the behaviors exhibited elongated intercopulatory and postejaculatory intervals. The administration of the putative dopamine-receptor agonist RDS-127 (2-N,N- di- n-propylamino-4,7-dimethoxyindane; 3 mg/kg, six minutes pretest) induced seminal emission ex copula and drastically reduced intromission frequency and ejaculation latency in copula, as well as effecting lesser reductions in the intercopulatory and postejaculatory intervals in two sequential copulatory series. RDS-127-induced seminal emission was effectively antagonized by pretreatment with the dopamine-receptor antagonist pimozide (250 μg/kg, two hours pretest), but not by pretreatment with metergoline. In contrast to seminal emission ex copula, pimozide pretreatment failed to antagonize the RDS-127 facilitation of ejaculatory behavior in copula. Metergoline pretreatment also failed to antagonize the RDS-127-induced facilitation of ejaculatory behavior in copula. However, RDS-127 prevented the suppressive effects of metergoline treatment, suggesting that RDS-127 has some agonistic action at serotonergic receptors. These results suggest that separate neurochemical mechanisms regulate seminal emission ex copula and ejaculatory behavior in copula, that RDS-127 induction of seminal emission ex copula may be mediated by dopaminergic receptors, and that RDS-127 facilitation of ejaculatory behavior in copula is mediated by receptors other than those accessible to blockade by the administered doses of pimozide and metergoline.

Experimental assessments of behavioral and anatomical components of female chacma baboon ( Papio ursinus) sexual attractiveness

Two experiments were carried out in order to separate the effects of the behavioral and the anatomical components of female sexual attractiveness in baboons. In the first experiment, two ovariectomized females were given increasing dosages of exogenous estradiol benzoate, and data were collected on their behavior as well as on male sexual arousal as assessed by the occurrence of coagulated seminal emissions of the type that result from masturbation. Male sexual arousal levels increased positively with the females' perineal swellings and appeared relatively unrelated to the females' behavior. In the second experiment, data were collected from five different groups of males in a systematic fashion across the period of a full menstrual cycle for their varied stimulus female partners. Behavior observations were carried out on the five different stimulus females, and ratings also were made of fluctuations in their perineal tumescence. The results of this experiment make it clear that male sexual arousal fluctuated across the study cycles in a fashion very similar to that of the perineal swellings of the stimulus females. Behavior was shown during all phases of the cycle, and, although it may have had a positive influence on male arousal during the follicular phase of the female's cycle, it had no apparent effect during the luteal phase. These results taken together establish for the first time that an estrogen stimulated female perineum per se has the potential to sexually arouse the male baboon. In addition, the data suggest that, although behavior may exert a positive effect on male arousal, in the absence of an estrogen stimulated perineum it is not sufficient to arouse males to masturbate. Finally the results establish that, although intact females appear to show behavior increases which may be arousing to males around the time of ovulation, these behaviors do not have to be shown by a female in order to arouse a male, provided she is swollen.

Central effects of RDS-127: Sexual behavior after intracerebroventricular administration and in vitro receptor binding studies

RDS-127, in a dose-related manner, induced seminal emission ex copula after intracerebroventricular (i.c.v.) administration. In mating tests initiated 6 min after i.c.v. administration, RDS-127 induced decreases in ejaculation latency and intromission frequency, with some rats ejaculating on the initial intromission. Additionally, penile reflexes were eliminated by 150 μg and 600 μg, but not by an intermediate dose. In in vitro radioligand binding studies, RDS-127 potently displaced [ 3H]DPAT binding to 5-HT 1A sites in rat cortex ( K i = 14 ± 4 nM) and was only moderately effective in displacing [ 3H]spiperone binding to dopaminergic D 2 sites in rat striatum. RDS-127 was essentially ineffective at 5-HT 1B sites labeled by [ 3H]5-HT in rat striatum ( K i = 13000 ± 4000 nM). These data demonstrate that centrally administered RDS-127 mimics the previously reported alterations in sexual behavior after systemic treatment and that RDS-127 is a high affinity 5-HT 1A agent with low affinity at the 5-HT 1B binding site.

Stimulation of spinal serotonergic receptors facilitates seminal emission and suppresses penile erectile reflexes

Penile erection and ejaculation are produced by spinal reflexes subjects to tonic control from the brain. This study examines the possible involvement of serotonergic transmission in the supraspinal modulation of such reflexes. The effects of two drugs which facilitate serotonergic transmission by different mechanisms, namely the direct receptor agonist, 5-methoxy-N, N′-dimethyltryptamine (5-MeODMT), and the reuptake inhibitor, zimelidine, were compared in intact and spinal rats. Results show that serotonergic stimulation in intact rats by either drug produces a dose-related increase in the incidence of seminal emission as well as a definite decrease of the display of erectile responses. In the spinal animals 5-MeODMT treatment reproduced both effects. By contrast, zimelidine, which needs functional nerve endings to exert its agonistic action, was ineffective in the spinal rats. This is interpreted to exclude a peripheral mechanism for the effects of the serotonin agonists on penile reflexes of intact animals and makes a strong case for a spinal site of action. We postulate the existence of serotonergic receptors located in the lower segment of the spinal cord which, when stimulated, trigger seminal emission and suppress erection.

Reproductive Biology of Paraplegics: Results of Semen Collection, Testicular Biopsy and Serum Hormone Evaluation

The fertility and urological status of 30 male paraplegics between 20 and 47 years old with lesions between the T2 and L3 levels were examined by studying serum hormone levels (estradiol-17β, testosterone, prolactin, and follicle-stimulating and luteinizing hormones), sperm and semen characteristics via testicular biopsy and rectal probe electro stimulation, and urodynamic evaluation. Of the patients 13 had reflexic, 4 hyperreflexic and 13 areflexic bladders. Nine of the 13 patients with reflexic and all 4 with hyperreflexic bladders had a positive external sphincter electro myogram with detrusor-sphincter dyssynergia. When catheters were not used to collect semen during rectal probe electro stimulation, retrograde semen flow into the bladder was the rule. A total of 22 patients could tolerate rectal probe electrostimulation, while 6 who could not were injured at the T12 level or lower. Seminal emissions were obtained from 35 of 42 studies in these 22 patients. Total sperm count was variable; in 22 studies it was greater than 20 million. Progressive motility usually was low; 77 per cent of the patients had less than 20 per cent motility. Of 13 biopsy specimens obtained 6 suggested normal testicular morphology, with tubule atrophy and spermatogenic activity only mildly reduced in 6 of the remaining 7. Serum testosterone and luteinizing hormone values were significantly higher (p less than 0.05) among the paraplegic patients than among intact male volunteers of the same age range. Other serum hormone levels were unchanged. Outcome of rectal probe electrostimulation and biopsy did not relate to the number of years of patient injury. Thus, the principal deterrent to the use of semen collected by rectal probe electro stimulation from paraplegics for artificial insemination resides in a predominantly low sperm motility. Suggestions for improvement of motility include 1) great care to minimize or prevent urinary tract infections, 2) selection of medications for urinary tract care that do not compromise sperm survival and 3) prevention of sperm stagnation in lower tract storage sites, perhaps by use of periodical rectal probe electro stimulation