To identify the effects of sertraline, a selective serotonin reuptake inhibitor, for the treatment of premature ejaculation (PE), changes in brain current-source density (CSD) of the high beta frequency band (22-30 Hz) induced by sertraline administration were investigated during audiovisual erotic stimulation. Eleven patients with PE (36.9 ± 7.8 yrs) and 11 male volunteers (24.2 ± 1.9 years) were enrolled. Scalp electroencephalography (EEG) was conducted twice: once before sertraline administration and then again 4 h after the administration of 50 mg sertraline. Statistical nonparametric maps were obtained using the EEG segments to detect the current-density differences in the high beta frequency bands (beta-3, 22-30 Hz) between the EEGs before and after sertraline administration in the patient group and between the patient group and controls after the administration of sertraline during the erotic video sessions. Comparing between before and after sertraline administration in the patients with PE, the CSD of the high beta frequency band at 4 h after sertraline administration increased significantly in both superior frontal gyri and the right medial frontal gyrus (Po0.01). The CSD of the beta-3 band of the patients with PE were less activated significantly in the middle and superior temporal gyrus, lingual and fusiform gyrus, inferior occipital gyrus and cuneus of the right cerebral hemisphere compared with the normal volunteers 4 h after sertraline administration (Po0.01). In conclusion, sertraline administration increased the CSD in both the superior frontal and right middle temporal gyrus in patients with PE. The results suggest that the increased neural activity in these particular cerebral regions after sertraline administration may be associated with inhibitory effects on ejaculation in patients with PE.

Lower urinary tract symptoms (LUTSs) and ED are clearly correlated, but to date no correlation with ejaculatory dysfunction (EjD) has been identified. Therefore, this study evaluated the impact of erectile function in men with LUTS on EjD and premature ejaculation (PE). Erectile function, PE and EjD of 239 men (mean age, 53.0±10.65 years), International Prostate Symptom Score (IPSS), International Index of Erection Function (IIEF), intravaginal ejaculatory latency time (IELT) and the seven-item Male Sexual Health questionnaire (MSHQ)-EjD were used to compare with the degree of LUTS. Ages were divided into five groups (o40, 40 --49, 50 --59, 60--69 and 470 years). The IPSS categorized patients into three symptom groups: mild, 1 --7; moderate, 8 --19; and severe, 419. ED was classified into five categories based on IIEF-EF scores: severe (0 --6), moderate (7 --12), mild-to-moderate (13--18), mild (19 --24) and normal (25 --30). The correlations among age, IIEF-EF, IELT and the MSHQ-EjD domain were studied through regression and cross-tabulation analyses. The results revealed that aging significantly affected each item of the MSHQ-EjD (Po0.05). The IIEF-EF domain was also correlated with each question on the MSHQ-EjD (Po0.05). PE (IELT o1 min) increased in incidence as patients got older but was not linked to IIEF-EF (P40.05). These results indicate that EjD is closely related to age and erectile function, and that PE is closely related to age, although PE is not related to erectile function. INTRODUCTIONRepresentative symptoms that may develop with aging include lower urinary tract symptoms (LUTSs) and ED. These two symptoms are not simply the result of aging, and they have a common pathophysiology. Thus, by treating one disease, a synergistic effect of treating the other disease may occur simultaneously. 1,2 A multinational questionnaire survey involving 12 815 men older than 50 years revealed that the two diseases are associated, and for those with ED, age and LUTS were more potent risk factors than diabetes, hypertension or hyperlipidemia. 3 Ejaculation is the process of sperm transport from the epididymis to the urethral meatus, resulting in the expulsion of semen. Ejaculation occurs in two phases: seminal emission and ejaculation proper, and they are mediated by sympathetic and parasympathetic inputs, respectively. When sexual stimulation is extremely intense, the autonomic impulses responsible for the emission phase exit the spinal cord at the T10 --L2 level via sympathetic chains, course into the pelvis as hypogastric outflow and onto the genital structures involved in ejaculation. Parasympathetic and somatic inputs from S2 to S4 then cause ejaculation proper, and antegrade ejaculation occurs. 4,5 If the ejaculation reflex takes place too quickly, it may induce premature ejaculation (PE). In contrast, if it is late, delayed ejaculation may occur. Abnormalities in the sympathetic nerves or deterioration in male hormone levels because of aging may reduce semen volume or ejaculation force and decrease the fre...

Higenamine mediates cardiotonic, vascular relaxation and bronchodilator effects. The relaxation effects and the mechanism of action of higenamine on the rat corpus cavernosum (CC) were assessed to investigate the effect of higenamine on penile erection. Strips of CC and aorta were used in organ baths for isometric tension studies. Tension was measured with isometric force transducers, and muscle relaxation was expressed as the percent decrease in precontraction induced by phenylephrine (PE). The relaxation reactions were investigated in an endothelial-denuded group and groups pretreated with N(G)-nitro-L-arginine methyl ester (NO synthesis inhibitor), propranolol (b-receptor blocker), indomethacin (COX inhibitor), glibenclamide (K þ ATP channel inhibitor), 4-aminopyridine (membrane potential-dependent potassium channel inhibitor) and methylene blue (guanylyl cyclase inhibitor) for 30 min. Intracavernous pressure (ICP) was assessed in rats after the intravenous administration of higenamine, and changes in guanosine 3 0 ,5 0 -cyclic monophosphate and adenosine 3 0 ,5 0 -cyclic monophosphate (cAMP) concentrations were measured on the basis of the higenamine concentration. Also, the combined reaction of higenamine and the phosphodiesterase type-5 (PDE-5) inhibitors was assessed. Higenamine induced relaxation of the CC and the aortic strips precontracted with PE in a dose-dependent manner. The CC was significantly more relaxed than the aortic rings in response to the same higenamine concentration (Po0.05). The CC relaxation reaction was suppressed by the b-receptor blocker propranolol. The cAMP concentration increased gradually with increased higenamine concentration (Po0.05). The ICP also increased with increased higenamine concentration in vivo (Po0.05). In the group pretreated with 10 À7 M higenamine, the relaxation reaction of CC induced by the PDE-5 inhibitor increased significantly, compared with CC exposed to the PDE-5 inhibitor but not pretreated with higenamine (Po0.05). In conclusion, higenamine induced relaxation of the rat CC in a dose-dependent manner. The effect may be mediated through b-adrenoceptors. The results suggest that higenamine may be valuable as a new lead compound for treating erectile dysfunction.