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Ejaculation control

Venlafaxine was approved by the FDA recently for the treatment of PD. Venlafaxine in doses of 75 to 225 mg/day reduced panic and anticipatory anxiety in short-term controlled trials. The most common side effects include anorexia, dry mouth, constipation, somnolence, tremor, abnormal ejaculation, and sweating.52... [Pg.615]

Increased concentrations of copper in ejaculates (16 mg/kg DW vs. 2 in controls) and liver (1435 mg/kg DW vs. 63). Sperm motility in test rams was significantly decreased, abnormalities were increased, and testes copper was elevated (96-101 mg/kg DW vs. 60-69 in controls)... [Pg.205]

Figure 4. The number of sperm inseminated during In-Pair Copulation (IPC) increases with the risk that the female contains sperm from another man. Risk of sperm competition is measured as the percent of time the couple have spent together since their last IPC (or the last 10 days, whichever is the shorter). Lower percent times together are associated with higher risks of sperm competition. Residual sperm numbers calculated from the parameters listed in Table 1 modified by exclusion of percent time together. All of the parameters listed are therefore statistically controlled (including hours since last ejaculation). Pseudo-replication of data is avoided by including only the first IPC inseminate per couple. Number of couples per data point as shown, F, 47 =5.7, P=0.022. Figure 4. The number of sperm inseminated during In-Pair Copulation (IPC) increases with the risk that the female contains sperm from another man. Risk of sperm competition is measured as the percent of time the couple have spent together since their last IPC (or the last 10 days, whichever is the shorter). Lower percent times together are associated with higher risks of sperm competition. Residual sperm numbers calculated from the parameters listed in Table 1 modified by exclusion of percent time together. All of the parameters listed are therefore statistically controlled (including hours since last ejaculation). Pseudo-replication of data is avoided by including only the first IPC inseminate per couple. Number of couples per data point as shown, F, 47 =5.7, P=0.022.
Residual numbers of sperm (millions) (Controlled for hrs since ejaculation) -71 16 -11+22 -1.5 0.93... [Pg.182]

The current data set contains 20 ejaculates (from 11 different men with 13 different women) which were collected under circumstances other than within a long-term partnership. There were three main situations (see Material and Methods). All were outside of a partnership (and thus qualify as EPCs) and all were situations in which the man would have had every reason, consciously and/or subconsciously, to assume that the woman already contained sperm from another man. Sperm competition theory, therefore, would predict that the male should inseminate an above average number of sperm (Parker 1990). However, neither actual sperm numbers, numbers controlled for hours since last ejaculation, nor numbers controlled for all of the factors in Table 1, supported the prediction (Table 2). On the contrary, males seemed to inseminate fewer sperm into women who were not their established partner. [Pg.182]

But not everything that norepinephrine and acetylcholine do is opposed. In one case, they cooperate. Acetylcholine stimulates penile erection by increasing blood flow to that organ. Norepinephrine controls ejaculation. In still other cases, the pharmacology of these neurotransmitters is unique. For example, acetylcholine induces urination by causing the bladder to constrict. Acetylcholine also induces secretion of saliva and tears. Norepinephrine has nothing to do with these functions. [Pg.297]

Long-lasting and specific effects of early odor experience have not yet been reported for many mammal species. In one experiment, rat mothers that raised male pups had their nipples and vagina scented with citral. When tested at 100 days of age, these males ejaculated sooner with sexually receptive, citral-scented females than with controls. Conversely, the latency to ejaculation of males reared with saline-treated mothers was shorter in matings with normal females than with citral-scented ones (Pillion and Blass, 1986). [Pg.243]

FIGURE 5—57. Serotonergic neurons descending down the spinal cord may be responsible for controlling certain spinal reflexes that are part of the sexual response, such as orgasm and ejaculation. [Pg.184]

Seminal emission and ejaculation are under control of the sympathetic nervous system. Emission results from a-adrenergic-mediated contraction of the epididymis, vas deferens, seminal vesicles, and prostate, which causes seminal fluid to enter the prostatic urethra. Concomitant closure of the bladder neck prevents retrograde flow of semen into the bladder, and antegrade ejaculation results from contraction of the muscles of the pelvic floor including the bulbocavemosus and ischiocavernosus muscles. [Pg.547]

Control of mating. A new type of sex pheromone was found present in Callosobruchus chlnensls, which is not a conventional sex attractant, but rather induces the male to extrude his genital organ and to effect copulation. A female dummy bearing the pheromone mimic, elicits copulation and ejaculation by the male. [Pg.219]

These data suggest that antidepressant-induced sexual dysfunction is more likely to be associated with agents that greatly potentiate 5HT neurotransmission. This notion is supported by the results of a 6-week doubleblind study of 24 men with premature ejaculation, in which paroxetine (20 mg/day) increased latency to ejaculation six-fold while mirtazapine (30 mg/day) had minimal effect (4). In a randomized, 8-week, double-blind, placebo-controlled study in 450 patients with major depression, fluoxetine (20 -0 mg/day) significantly impaired sexual function, while the noradrenaline re-uptake inhibitor reboxetine had no effect (5). [Pg.3]

The ability of SSRIs to cause delayed ejaculation has been used in controlled trials of men with premature ejaculation (61,62). Of the SSRIs, paroxetine and sertraline produced the most benefit in terms of increase in time to ejaculation, but fluvoxamine did not differ from placebo. Clomipramine was more effective than the SSRIs but caused most adverse effects. From a practical point of view many patients might prefer to take medication for sexual dysfunction when needed rather than on a regular daily basis, and it would be of interest to study the beneficial effects of SSRIs on premature ejaculation when used in this way. [Pg.42]

Kim SC, Seo KK. Efficacy and safety of fluoxetine, sertraline and clomipramine in patients with premature ejaculation a double-blind, placebo controlled study. J Urol 1998 159(2) 425-7. [Pg.51]

Waldinger MD, Hengeveld MW, Zwinderman AH, Olivier B. Effect of SSRI antidepressants on ejaculation a double-blind, randomized, placebo-controlled study with fluoxetine, fluvoxamine, paroxetine, and sertraline. J Clin Psychopharmacol 1998 18(4) 274-81. [Pg.51]

Their most frequent adverse events (nausea, somnolence, dry mouth, increased sweating) are mainly transient and mostly mild to moderate (3). In terms of adverse effects escitalopram appears to be equivalent to citalopram. For example, in placebo-controlled trials, escitalopram produced unwanted effects typical of the SSRI class, including nausea (15%), ejaculation disorders (9%), insomnia (9%), diarrhea (8%), somnolence (7%), dry mouth (6%), and dizziness (6%). [Pg.53]

Escitalopram was efficacious in patients with major depressive disorder in short-term, placebo-controlled trials, three of which included citalopram as an active control, and in a 36-week study in the prevention of relapse in depression (7). It has also been used to treat generalized anxiety disorder, panic disorder, and social anxiety disorder. Results also suggest that, at comparable doses, escitalopram demonstrates clinically relevant and statistically significant superiority to placebo treatment earlier than citalopram. The most common adverse events associated with escitalopram include nausea, insomnia, disorders of ejaculation, diarrhea, dry mouth, and somnolence. Only nausea occurred in more than 10% of patients taking escitalopram. [Pg.53]

Drugs that potentiate serotonin function can cause ejaculatory delay in men, and this has led to the use of SSRIs to treat premature ejaculation (SEDA-26, 13). Venlafaxine is also reported to cause problems with ejaculation during routine use and its efficacy has been studied in a placebo-controlled, crossover study in 31 men with ejaculation latencies of less than 2 minutes (25). Both placebo and venlafaxine (75 mg/day of the XL formulation) significantly increased latency to ejaculation over baseline, placebo by 2 minutes and venlafaxine by 3 minutes there was no difference between the two treatments. The authors concluded that venlafaxine is not effective for the management of premature ejaculation. However, the small number of subjects studied and the large placebo effect makes this conclusion tentative. It does appear, however, that the effect of venlafaxine on ejaculation delay is probably less striking than, for example, that of paroxetine. [Pg.117]

Kilic S, Ergin H, Baydinc YC. Venlafaxine extended release for the treatment of patients with premature ejaculation a pilot, single-blind, placebo-controlled, fixed dose crossover study on short-term administration of an antidepressant drug. Int J Androl 2005 28 47-52. [Pg.121]

All drugs that interfere with sympathetic autonomic activity, including diuretics, can potentially interfere with male sexual function, expressed as a failure of ejaculation or difficulty in sustaining an erection. Nevertheless, placebo-controlled trials have emphasised how common a symptom this is in the untreated male popialation (approaching sometimes 20-30%). It is also likely that hypertension itself is associated with an increased risk of sexual dysfunction since loss of NO production by the vascular endothelium is an early feature of the pathophysiology of this disease. Laying the blame on antihypertensive medication is probably... [Pg.492]

The detrusor, whose smooth muscle fibres comprise the body of the bladder, is innervated mainly by parasympathetic nerves which are excitatory and cause the muscle to contract. The internal sphincter, a concentration of smooth muscle at the bladder neck, is well developed only in the male and its principal hmction is to prevent retrograde flow of semen during ejaculation. It is rich in aj-adrenoceptors, activation of which causes contraction. There is an abvmdant supply of oestrogen receptors in the distal two-thirds of the female urethral epithelium which degenerates after the menopause causing loss of urinary control. [Pg.543]

The adverse effects of thiazide and thiazide-like diuretics on male sexual function include reduced libido, erectile dysfunction, and difficulty in ejaculating. The exact incidence of sexual dysfunction in patients taking diuretics is poorly documented, perhaps because of the personal nature of the problem and the reluctance of patients and/or physicians to discuss it. However, these abnormalities have been reported with incidence rates of 3-32%. The true incidence of sexual dysfunction probably lies closer to the lower end of this range (119). In a meta-analysis of 13 randomized, placebo-controlled trials conducted over a mean of 4 years the NNH (number needed to harm) for erectile impotence with thiazide diuretics in hypertension was 20 and the relative risk was 5.0 (120). [Pg.1161]


See other pages where Ejaculation control is mentioned: [Pg.321]    [Pg.488]    [Pg.489]    [Pg.175]    [Pg.179]    [Pg.179]    [Pg.187]    [Pg.225]    [Pg.446]    [Pg.198]    [Pg.205]    [Pg.230]    [Pg.664]    [Pg.836]    [Pg.31]    [Pg.178]    [Pg.152]    [Pg.239]    [Pg.195]    [Pg.137]    [Pg.246]    [Pg.321]    [Pg.2238]    [Pg.338]    [Pg.1536]    [Pg.85]    [Pg.86]   


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