A sexually competent male must have a series of events occur and multiple mechanisms intact for normal erectile function. He must 1) have desire for his sexual partner (libido), 2) be able to divert blood from the iliac artery into the corpora cavernosae to achieve penile tumescence and rigidity (erection) adequate for penetration, 3) discharge sperm and prostatic/seminal fluid through his urethra (ejaculation), and 4) experience a sense of pleasure (orgasm). A man is considered to have ED if he cannot achieve or sustain an erection of sufficient rigidity for sexual intercourse. Most men, at one time or another during their life, experience periodic or isolated sexual failures. However, the term “impotent” is reserved for those men who experience erectile failure during attempted intercourse more than 75% of the time.
When these drugs don't work, there are other options. Medications that dilate blood vessels, such as alprostadil, can be injected or deposited in the penis; they work in more than 80 percent of men with diabetes. Beyond that, penile implants can be an effective surgical solution. Implants are either malleable rods, which can be manually adjusted to the desired position, or inflatable cylinders that fill with fluid when a pump under the skin of the scrotum is pressed.

Despite its limitations in detecting CVD without significant stenosis, EST (with or without imaging) can further define the cardiovascular risk in patients with ED and no overt CAD and may be particularly helpful for identifying silent CAD in patients with diabetes. Chemical stress tests are appropriate for patients who cannot complete an EST or in whom ECG is non-interpretable. In patients with established CVD, an interpretable EST is mandatory in the indeterminate risk category and is at the discretion of the cardiologist in the low risk category (Table 3B), since it determines exercise ability and estimates cardiovascular risk associated with sexual activity.
“I’m hoping this study will drive that (tie) a little bit harder and faster so that physicians will routinely be including ED when they’re screening patients for cardiovascular disease,” he said. “Doctors should ask the question and consider whether hardening of the arteries is occurring, ask about family history and signs or symptoms like chest pain with exertion, and spend the requisite amount of time to find out what’s going on.”
Inflatable prostheses are complex mechanical devices that imitate the natural process of erection. Parts are inserted surgically into the penis and scrotum, and activated by squeezing. When erection is no longer desired, a valve on the pump is pressed, and the penis becomes flaccid. Self-contained single-unit prostheses are similar to the inflatable types, but more compact. The entire device is implanted into the penis. When erection is desired, the unit is activated by either squeezing or bending, depending on which of the two types of self-contained prostheses is used.
The drugs you take to lower your blood pressure may earn you lower marks in the bedroom, by leading to a bout of erectile dysfunction (ED), or the inability to get or maintain an erection during sex. High blood pressure medications such as beta blockers and diuretics do their life-saving job by lessening blood flow to your vital organs—and that includes down under. Less blood flow means no erection. The good news for guys is that not all high blood pressure medication cause ED. Talk with your doctor about switching to the ones that don't.
"The answer to the question, 'Can patients with heart disease safely have sex?' is almost always 'Yes,' unless they have such bad heart failure or severe artery disease that even a moderate amount of exertion will cause terrible chest pain," says Richard Stein, MD, who is director of preventive cardiology at New York City's Beth Israel Hospital. "And if that is the case, sex is probably the last thing on their minds anyway."
Does drinking water improve erectile dysfunction? Erectile dysfunction or ED is a common concern for men. Everyday factors, such as hydration levels, may affect a person's ability to get or maintain an erection. Drinking water may, therefore, help some men with ED. In this article, learn about the link between hydration and ED, and other factors that can cause ED. Read now
Crossref | Google ScholarSee all References A 1985 study found that ED accounted for 400,000 outpatient visits and 30,000 hospital admissions per year in the United States, with a direct total cost of $146 million.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61

Crossref | PubMed | Scopus (23) | Google ScholarSee all References Similar to sildenafil, vardenafil produces a slight hypotensive effect with an average maximal decrease in blood pressure level of 5 to 10 mm Hg.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446


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Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
In DM patients with a documented androgen deficiency, testosterone replacement may correct or facilitate the treatment of ED.7 A transdermal testosterone gel or patch, or intramuscular testosterone cypionate are the alternatives. Oral testosterone is contraindicated in the United States due to hepatotoxicity, but a new product has been developed that allows for buccal absorption of testosterone. Thyroid supplements rarely alleviate EDDM.
Erections are extremely complicated and surprisingly fragile. Erections involve chemical signals, nerve impulses, complicated blood pressure changes, and overall fitness in systems ranging from your heart and hormones to your mood. When medication changes how one of these factors works—like blood pressure drops or depression medication—ED is a common side effect. The problem with these completely predictable medically induced side effects is how people react.
The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels.

Unfortunately, government agencies often are slow to respond to new scientific information and economic and political forces make it difficult for our population to receive clear information informing them that heart disease is nutritionally induced and totally avoidable with dietary excellence. Sadly, even the American Heart Association advocates a diet that has been shown to actually increase heart disease.
Montorsi F,  Briganti A,  Salonia A,  Rigatti P,  Margonato A,  Macchi A,  Galli S,  Ravagnani PM,  Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease, Eur Urol , 2003, vol. 44 (pg. 360-364)https://doi.org/10.1016/S0302-2838(03)00305-1

Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References However, subsequent studies of older patients who had sexual intercourse in their home and were monitored with ambulatory ECG reported significantly lower heart rates and blood pressure levels.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F
With early detection, doctors can suggest preventive measures like statins, blood pressure meds, revamping eating habits and getting more exercise. Try these two exercises that can cut your risk of heart disease in half. The study researchers told Science Daily, “Our study supports a more aggressive CVD risk assessment and management for persons with erectile dysfunction, including young men who may otherwise be categorized as low-risk due to their young ages.” Check out the sexual health conditions affecting millennial men.
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Another study evaluated 32 hypertensive men with ED and 78 normotensive men with ED with regard to age, body mass index, hormonal profile, penile arterial flow, risk factors for arterial disease, psychiatric disease, and neurologic disease measured by pudendal nerve conduction studies.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862

The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Originally evaluated as a mild preload reducer and antianginal agent in its early phases of development, sildenafil's effect on male and female genitalia became quickly apparent.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Crossref | PubMed | Scopus (539) | Google ScholarSee all References After adjusting for age, vascular disease, psychiatric disease, hormonal factors, and marital status, a study of 4462 US Army veterans aged 31 to 49 years found an odds ratio of 1.8 for the risk of developing ED in men who smoked.26x26Mannino, DM, Klevens, RM, and Flanders, WD. Cigarette smoking: an independent risk factor for impotence?. Am J Epidemiol. 1994; 140: 1003–1008
Erectile dysfunction (ED), or impotence, is when a man has difficulty getting or maintaining a strong enough erection for sexual intercourse or other sexual activity. It can be caused by stress, anxiety or excessive alcohol consumption. But it can also be a symptom of an underlying condition such as atherosclerosis (narrowing of the arteries), diabetes or high blood pressure. Some medications can cause erectile dysfunction, for example beta-blockers and diuretics (commonly used to treat a variety of heart-related conditions such as high blood pressure and heart failure).

According to Harvard Special Health Report Erectile Dysfunction, one study in the European Heart Journal looked at men newly diagnosed with heart disease, but without ED, who started treatment with the beta-blocker atenolol (Tenormin). Some of the study participants were told about the sexual side effect of the blood pressure drug, and ED was reported by almost one-third of the participants. In contrast, among those who were not told the drug's name or its side effects, only 3% said they experienced ED.
Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection for satisfactory sexual performance. The prevalence of ED has been estimated as nearly 40% of men >40 years of age1 although these figures are contested.2 ED increases in frequency with age and is estimated to affect 15% of men aged 40–50 years, 45% of men in their 60s and 70% of men older than 70 years.3 Successful erection is a complex system involving reflex action (peripheral nerves and spinal cord), the limbic system (psychogenic stimuli) and the release of nitric oxide. Adequate levels of testosterone are required, and hence an intact hypothalamic/pituitary/testicular axis. Hence, ED can result from disease or treatment that produces hormonal deficiency, neurological impairment, problems with penile blood flow, disorders of tissue mechanics, psychological factors or any combination of these.
There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.
This may seem like a lot to manage at a glance, however, just focus on one step at a time. If it is more exercise you want to start with, park your car further away from the front door at work so you have to walk a little more every day. Or go out on a walk to make your phone calls.  If you need to eat better,  try low-fat meat and chicken for lunch. Just keep it simple and don’t try to do it all at once.

Although DM patients often correctly assume that their ED is of organic origin, a psychogenic component should be considered, especially in the younger patient. If this is the case, the patient may benefit from psychosocial therapy that includes anxiety reduction and desensitization, cognitivebehavioral intervention, sexual stimulation techniques, and interpersonal assertiveness with couples communication training.6 Not all healthcare providers offer these options. Freudian-based psychotherapy for EDDM has not been proved to be efficacious.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References No data suggested adverse interactions between sildenafil and other drugs commonly used in the treatment of coronary artery disease, such as aspirin, heparin, or narcotics.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.
Severe testosterone deficiency, known as “hypogonadism,” is present in approximately 2–35% of men with erectile dysfunction.19 However, lesser degrees of deficiency are common, perhaps present in the majority, depending on the definition of “low” applied, the method of measurement, and the parameter being used to define testosterone (total, free, or bioavailable) deficiency.19,20 Most authorities agree that a total testosterone level below 300 ng/dL is clearly low, and that 300–400 ng/dL is low to low-to-normal. Most studies using testosterone replacement for erectile dysfunction have attempted to achieve blood levels of 450–850 ng/dL.
Erectile dysfunction started to become a household term after scientists discovered a drug to treat it. Nowadays, as anyone who watches TV can attest, there are several different medications for ED. Fifty to 70 percent of men with type 1 or type 2 diabetes respond to a class of drugs—including sildenafil (Viagra), var­denafil hydrochloride (Levitra), and tadalafil (Cialis)—called phosphodiesterase-5 inhibitors.
Crossref | PubMed | Scopus (165) | Google ScholarSee all References Typically, the response to sexual activity is no more than an increase in heart rate to 130 beats/min and an increase in systolic blood pressure level to 170 mm Hg.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
In the vessels that supply the heart, healthy arteries enlarge in diameter up to 50% during exercise when sufficient nitric oxide is present. Because of its brief half-life, a continual supply of nitric oxide is required for optimal effect. If the supply of nitric oxide is inadequate, endothelial dysfunction—a core factor in heart disease—is made worse. Endothelial dysfunction can trigger the growth of coronary plaque.8
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Erectile dysfunction is a common physiological disorder. According to estimates from the National Institutes of Health, ED affects 10 million to 20 million men in the United States; another 10 million men are affected by partial ED, defined as present but diminished erectile function.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90
In an open-label study, 8 patients monitored with a Swan-Ganz catheter were given a total of 40 mg of sildenafil in 4 intravenous transfusions (the equivalent of 1 to 3 times the plasma concentration after an oral dose of 100 mg).62x62Jackson, G, Benjamin, N, Jackson, N, and Allen, MJ. Effects of sildenafil citrate on human hemodynamics. Am J Cardiol. 1999; 83: 13C–20C
Despite its limitations in detecting CVD without significant stenosis, EST (with or without imaging) can further define the cardiovascular risk in patients with ED and no overt CAD and may be particularly helpful for identifying silent CAD in patients with diabetes. Chemical stress tests are appropriate for patients who cannot complete an EST or in whom ECG is non-interpretable. In patients with established CVD, an interpretable EST is mandatory in the indeterminate risk category and is at the discretion of the cardiologist in the low risk category (Table 3B), since it determines exercise ability and estimates cardiovascular risk associated with sexual activity.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Originally evaluated as a mild preload reducer and antianginal agent in its early phases of development, sildenafil's effect on male and female genitalia became quickly apparent.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N

Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Neurological (nerve and brain) diseases: The nervous system plays a vital part in achieving and maintaining an erection. It is common for men with conditions such as stroke, multiple sclerosis (MS), Alzheimer’s disease, Parkinson’s disease, and spinal cord injuries to experience ED. This is due to an interruption in the transmission of nerve impulses between the brain and the penis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
If the cause is believed to be organic but not hormonal, or if the patient defers psychological intervention, he can be offered the VCD or oral drug therapy. EDDM patients on organic nitrates or who have experienced or are concerned about potential adverse reaction to PDE-5 inhibitors are suitable candidates for the VCD. The VCD induces functional rigidity in 75% of patients with diabetes with autonomic neuropathy. Some patients or their partners may reject or discontinue the use of the VCD because it induces an unnatural erection, causes bruising and numbness of the penis, and or inhibits antegrade ejaculation.8 

Abstract | Full Text | Full Text PDF | PubMed | Scopus (395) | Google ScholarSee all References Phosphodiesterase type 5 is primarily responsible for the breakdown of cGMP in cavernosal tissues. The inhibition of PDE-5 by sildenafil therefore causes continued activation of the NO-cGMP pathway in the cavernosal tissue, thereby improving erectile function.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
Diabetes mellitus (DM) is strongly associated with an increased risk of erectile dysfunction (ED), the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance, but this condition can be successfully treated in the majority of diabetes patients. ED is present in 32% of type 1 and 46% of type 2 DM patients. Several population- based studies of ED prevalence calculated the odds ratios for the association between ED and various chronic diseases. An odds ratio must be sufficiently greater than 1.0 to identify an increased risk. Diabetes has an odds ratio, ED risk multiplier of 4.1, compared with 1.7 for hyperlipidemia and 1.6 for hypertension. Erectile dysfunction in diabetes mellitus (EDDM) patients has been considered to have an organic etiology. Healthcare providers have long realized that ED can be the first symptom of DM.
Diuretics: Also called water pills, this medication is a common treatment for reducing blood pressure. They work by getting rid of unnecessary water and salt in the urine. This essentially helps lower blood pressure and can make it easier for the heart to pump blood. Unfortunately, diuretics can reduce the blood flow to the penis, making erections difficult to achieve. Zinc levels have been known to diminish due to diuretic use, which may lead to a decreased production of overall testosterone.
If you can't take one of these oral medications, your physician may have you try Caverject (alprostadil for injection), a hormone that you inject into your penis using a fine needle, or Muse (alprostadil urogenital), a tiny suppository that you insert into the tip of the penis. Both of these will bring on an erection within five to 15 minutes without sexual stimulation.
The truth is medication or psychosexual counselling are the first treatments a doctor will suggest because they’ve been proven to work. If a doctor has approved a medication for you then it’s safe. If you would still like to see if herbal supplements work for you, then there is a list below of supplements thought to work for erectile dysfunction. Just before you invest your money in them, remember they aren’t proven to work:
The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Hypertension per se and antihypertensive drug therapy may contribute to the development of erectile dysfunction in patients with arterial hypertension. The management of erectile dysfunction in hypertensive patients is tricky and should take into account the different effects of antihypertensive drug categories on erectile function. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, PDE-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease and better characterize the relevant risk with obvious benefits for cardiovascular disease prevention.
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.

Surgery for erectile dysfunction is usually considered only after all other options have failed. The two surgical options include the insertion of a semi-rigid rod or the implantation of a three-piece inflatable prosthesis. Penile prosthesis implantation has low infection, complication, and malfunction rates. However, since placement of an implant requires permanent injury to the erectile tissue of the penis, implant treatment is considered irreversible.
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