[Male sexual insufficiency].

There are patients who complaint the loss of sexual desire, loss of erection, absence of emission, absence of orgasm, and premature ejaculation. When the primary disturbance is in the producing or releasing process of testosterone in the testis, it increases the gonadotropic stimulation and results in the hypergonadotropic hypogonadism. Hypogonadotropic hypogonadism, in contrast, suggests that the disturbance in the hypophysis or hypothalamus. Patients who have the primary disturbance in the hypothalamus sometimes do not respond to LHRH, but repeated pulsatile LHRH stimulation induces the response. LH-testosterone is known to be the main axis of sexual function. However, growth hormone (GH) also has an important role. GH is necessary for adults, not only for children. Its deficiency arises easy fatiguability, loss of sexual desire, loss of erection, and oligo- or azoospermia. Erectile dysfunction is frequently caused by vascular, neurological and psychosomatic disorders. A variety of drugs are known to cause male sexual insufficiency. Many environmental factors and stress may affect the release of LH and GH, and therefore disturb the male sexual function.

Effects of Ilexonin A on circulatory neuroregulation.

Ilexonin A (IA), a pentacyclic triterpene, has been semisynthesized in china for the first time. It is extracted from the root of Ilicis pubescentis, a commonly used herbal medicine in Guangdong for the treatment of cardiovascular, cerebrovascular and peripheral vascular diseases and heart failure with satisfactory effects. The pharmacokinetic studies indicated that the elimination half-life after oral and i.v. dosing were 17.7 +/- 2.4 h and 22.5 +/- 2.9 h respectively. The total clearance was 4.6 +/- 0.51/h. The bioavailability of IA capsules was 0.39 +/- 0.14 and LD50 was 234 mg/Kg. We have adopted modern techniques, including cellular electrophysiology, isotope tracing methods, molecular biology, electromicroscopy, etc., to probe into the pharmacologic mechanisms of the effects of IA on cardiovascular system. The results indicated that IA can increase the contractility of isolated guinea pig auricular myocardium, attenuate vascular smooth muscle tension induced by noradrenaline in the rabbit aorta. IA can exert a biphasic regulatory effect on arterial blood pressure. IA also can prolong A-V duration of Hiss bundle electrograph (HBE) in rabbits and prolong the action potential duration and the effective refractory period (ERP) of myocardial cells in guinea pigs. The results showed that IA can increase the cAMP content in the smooth muscle of aorta and exert a calcium-blockade effect. Therefore, the peripheral resistance vessels are relaxed and the cardiac afterload is lowered. IA-blocked calcium channels are correlated with both the potential-dependent channel and the receptor operated channel in vascular smooth muscles. IA also increases the cAMP content of myocardium and accelerates the cellular calcium influx and efflux, and this may be responsible for the direct mechanism of the positive inotropic action of IA. Under electron microscopy, it is observed that IA can alleviate the defect of succinate dehydrogenase in the myocardial mitochrondria of rabbit chronic congestive heart failure (CF) model and reduce the microstructural damage of the failed myodardium, therefore the anoxic tolerance of myocardium is increased, the effect of IA on the platelet stretching activity and microstructure in the patients with CF is also studied. It is found that IA can reduce the hypercoagulability of blood, decrease the severity of blood stagnation and improve the status of microcirculation. Effects of IA introventricular and cardiovascular central microinjection (nucleus tractus solitarius, paraventricular nucleus) on arterial blood pressure and heart rate were studied. It demonstrated that IA possess circulatory neuroregular effects by the medium of alpha-receptor and beta-receptor of cardiovascular motoneurons.