Sexual stimulation causes the release of neurotransmitters from cavernosal nerve endings and relaxation factors from endothelial cells lining the sinusoids. NOS produces NO from L-arginine, and this, in turn, produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP), which work via calcium channel and protein kinase mechanisms (see the image below). This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow.
To examine what is known about the demographics, etiology, risk factors, pathophysiology, diagnostic assessment, treatments (both generic and cause-specific), and the understanding of their consequences by the public and the medical community, the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research of the National Institutes of Health, in conjunction with the National Institute of Neurological Disorders and Stroke and the National Institute on Aging, convened a consensus development conference on male impotence on December 7-9, 1992. After 1 1/2 days of presentations by experts in the relevant fields involved with male sexual dysfunction and erectile impotence or dysfunction, a consensus panel comprised of representatives from urology, geriatrics, medicine, endocrinology, psychiatry, psychology, nursing, epidemiology, biostatistics, basic sciences, and the public considered the evidence and developed answers to the questions that follow.
Only a small proportion of cases of erectile dysfunction are caused by hormone abnormalities. The most frequent hormone abnormality is a reduced level of the male sex hormone testosterone required to get an erection which can be restored by appropriate hormone replacement. It's unwise to take testosterone preparations unless you've had tests that confirm a deficiency.
#4 You’re just plain turned off. It happens. Whether it’s the weight your partner has put on, the realization that you’re having period sex, or you’re just not getting what you need in the bedroom, at some point in your life, you’re going to be turned off enough to lose *or be unable to attain* your hard-on. [Read: Not attracted to your girlfriend anymore? The why and the fixes]
2 inability of the adult male to achieve or sustain a penile erection or, less commonly, to ejaculate after achieving an erection. Several forms are recognized. Functional impotence has a psychological basis. Organic impotence includes vasculogenic, neurogenic, endocrinic, and anatomical factors. Anatomical impotence results from physically defective genitalia. Atonic impotence involves disturbed neuromuscular function. Poor health, old or advancing age, drugs, smoking, trauma, and fatigue can induce impotence. Also called erectile dysfunction, impotency. impotent, adj.
Diabetes mellitus: Erectile dysfunction tends to develop 10 to 15 years earlier in diabetic men than among nondiabetic men. The increased risk of erectile dysfunction among men with diabetes mellitus may be due to the earlier onset and greater severity of atherosclerosis (hardening of the arteries) that narrows the arteries and thereby reduces the delivery of blood to the penis. Atherosclerosis can affect the arteries in the penis, as well as the arteries in the pelvis that supply the penile arteries. Diabetes mellitus also causes erectile dysfunction by damaging nerves that go to the penis, much like the effect of diabetes on nerves in other areas of the body (diabetic neuropathy). Diabetes can also affect the muscles in the penis, leading to troubles with erections. Smoking cigarettes, obesity, poor control of blood glucose levels, and having diabetes mellitus for a long time further increase the risk of erectile dysfunction in people with diabetes.
The first stem cell study for the treatment of ED was published in 2004. This study used embryonic stem cells to treat ED. At this time, there is a total of 36 published basic studies assessing stem cell therapy for ED, with two clinical trials. The mechanism of action of stem cells is to generate angiogenesis with subsequent increase in cavernosal smooth muscle cells within the corporal bodies.46
A lot of the time, the issue is a combination of both. For instance, cortisol – which is an important steroid hormone in the body – is released in greater amounts when we're stressed. It's supposed to briefly shut down non-essential functions like reproduction and fighting off illnesses whilst you deal with the danger at hand. However, the chronic and ongoing stress of modern life increases our background cortisol levels, activating the sympathetic system and stopping an erection.
On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.
It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.
Half of all men between the ages of 40 and 70 will experience erectile dysfunction. While the problem doesn't cause heart disease, the two often occur together – study after study has shown that men with ED are dramatically more likely to develop heart disease and have a heart attack or stroke. One German study from 2010 found men with erectile dysfunction are twice as likely to die within the next two years as those without, prompting some experts to call the phenomenon "the canary in the trousers".
There are, as you listen to all of the advertisements, if your erection lasts for more than four hours, there are very, very unusual cases where that can happen. There are very rare cases of visual problems. There are even rarer cases of hearing problems. But with every medication, there always a potential downside. But the absolute contraindication is an unstable medical condition, an unstable cardiovascular condition, being on nitrates.
Estimates of the prevalence of impotence depend on the definition employed for this condition. For the purposes of this consensus development conference statement, impotence is defined as male erectile dysfunction, that is, the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Erectile performance has been characterized by the degree of dysfunction, and estimates of prevalence (the number of men with the condition) vary depending on the definition of erectile dysfunction used.
Recently, the US Food and Drug Administration (FDA) has issued a safety announcement regarding TRT. In part it reads ‘The benefit and safety of these medications have not been established. We are also requiring these manufacturers to add information to the labeling about a possible increased risk of heart attacks and strokes in patients taking testosterone.’37
Watts and coworkers, in their review article, make several points about this ED/CAD nexus. Endothelial dysfunction is present in both CVD and ED, and is linked through the NO mechanism. The authors note that PDE5 inhibitors improve endothelial function and have a salutary effect on both CVD and ED. Both ED and cardiac disease respond to modifications in lifestyle as well as pharmacologic manipulation. These authors also report that the presence of ED gives the clinician an opportunity to assess CVD and prevention as well.20
Hypogonadism may be suggested by the patient's general appearance. If testosterone deficiency antedates puberty, as in Klinefelter's syndrome, eunuchoid proportions—defined as an arm span 5 cm or more in excess of height, or a sole-to-pubis length exceeding crown-to-pubis length by more than 2 cm—may be present. In postpubertal males whose testosterone levels are markedly depressed, the secondary sexual characteristics may become atrophic. Testicles less than 4 cm in length or a prostate gland that is smaller than expected may be the only clues on physical examination to a pituitary tumor with secondary hypogonadism.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
Sildenafil (Viagra) was the first oral phosphodiesterase type 5 (PDE5) inhibitor approved by the FDA in the United States for the treatment of erectile dysfunction (it is not approved for women). Sildenafil inhibits PDE5, which is an enzyme that destroys cGMP. By inhibiting the destruction of cGMP by PDE5, sildenafil allows cGMP to accumulate. The cGMP in turn prolongs relaxation of the smooth muscle of the corpora cavernosa. Relaxation of the corpora cavernosa smooth muscle allows blood to flow into the penis resulting in increased engorgement of the penis. In short, sildenafil increases blood flow into the penis and decreases blood flow out of the penis.
The history can be useful in distinguishing organic from psychogenic impotence (Table 187.1). The patient with organic impotence describes problems with erection that progress over months to years. At first, the patient will have partial erections or seemingly firm erections that become flaccid during intercourse. With time, total erectile failure ensues. Organic impotence is constant and nonselective, meaning it is not better or worse with any specific partner or any type of stimulation.
This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the patient's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
Men with a rare heart condition known as long QT syndrome should not take vardenafil since this may lead to abnormal heart rhythms. The QT interval is the time it takes for the heart's muscle to recover after it has contracted. An electrocardiogram (EKG) measures the QT interval. Some people have longer than normal QT intervals, and they may develop potentially life-threatening abnormal heart rhythms, especially when given certain medications. Men with a family history of long QT syndrome should not take vardenafil, as it is possible to inherit long QT syndrome. Furthermore, vardenafil is not recommended for men who are taking medications that can affect the QT interval such as quinidine (Quinaglute, Quinidex), procainamide (Pronestyl, Procan-SR, Procanbid), amiodarone (Cordarone), and sotalol (Betapace).
The inflatable type of device consists of cylinders that are implanted in the corpora cavernosa, a fluid reservoir implanted in the abdomen, and a pump placed in the scrotum. The man squeezes the pump to move fluid into the cylinders and cause them to become rigid. (He reverses the process by squeezing the pump again.) While these devices allow for intermittent erections, they have a slightly higher malfunction rate than the silicon rods.
I am a woman who is currently in menopause. My sex drive has increased and i believe that it can equate to a teenage boy. My s.o. has erection dissatification. He can not penetrate. He prefers oral. He will become erect and orgasm. He works very hard to please me but sometimes I want intercourse. It makes me feel like he isnt attracted to me. I have been with him for quite some time and believe he has always had this problem. I dont understand why. I understand when you say that your wife has no interest. It can be hurtful.
Stress is another factor that can be a cause or effect of ED. If you're stressed at work, at home, and in your relationships, it's going to take a toll on your sexual function. Your mind is elsewhere, and relaxing when you finally make it between the sheets is a long shot. Now you’re stressed because you can’t get it up (talk about the ultimate catch-22), so you're stuck in this sad, frustrating cycle. “ED really affects the psyche of a guy, regardless of the etiology, Gittens says. “If you have a problem getting an erection one night, you’re probably going to be anxious and worried your partner might see you as less of a man the next time you try to get an erection.” There's a pill that will help with this, and it's not promoted on television with middle-aged men in sports cars. It's a damn chill pill.