Instead of the hesitation with which he had accosted the cardinal a quarter of an hour before, there might be read in the eyes of the young king that will against which a struggle might be maintained, and which might be crushed by its own impotence, but which, at least, would preserve, like a wound in the depth of the heart, the remembrance of its defeat.
Because adequate arterial supply is critical for erection, any disorder that impairs blood flow may be implicated in the etiology of erectile failure. Most of the medical disorders associated with erectile dysfunction appear to affect the arterial system. Some disorders may interfere with the corporal veno-occlusive mechanism and result in failure to trap blood within the penis, or produce leakage such that an erection cannot be maintained or is easily lost.

My boyfriend has a hard time getting and staying hard. It's obviously a difficult situation to talk about, but he says he feels pressure when he's with me (versus previous random hookups he wasn't invested in), so he psyches himself out. When we do have sex, I'm almost always really satisfied and I care a lot about him, both things I express in and outside of the bedroom. But the situation seems to be only getting worse. We've stopped having sex during the week because our busy lives mean we don't have an hour or more to devote to sex (which is sometimes what it takes), or we can't have sex at all because of what he's experiencing. I'm afraid this is going to continue to get worse, not only sexually but emotionally in our relationship. How can I help him fix this, and reassure him in the meantime that I care about him and want to support him?
The physical side effects of chemotherapy are usually temporary and resolve within one to two weeks after stopping the chemotherapy. However, chemotherapy agents, such as Ciplatin or Vincristine, may interfere with the nerves that control erection leading to possible impotence. Make sure you discuss potential side effects of cancer chemotherapy with your doctor or healthcare provider.

The dorsal artery provides for engorgement of the glans during erection, whereas the bulbourethral artery supplies the bulb and the corpus spongiosum. The cavernous artery effects tumescence of the corpus cavernosum and thus is principally responsible for erection. The cavernous artery gives off many helicine arteries, which supply the trabecular erectile tissue and the sinusoids. These helicine arteries are contracted and tortuous in the flaccid state and become dilated and straight during erection. [9]
The most important organic causes of impotence are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this is somewhat less frequent but can often be helped. In psychological impotence, there is a strong response to placebo treatment.
This consensus development conference on male erectile dysfunction has provided an overview of current knowledge on the prevalence, etiology, pathophysiology, diagnosis, and management of this condition. The growing individual and societal awareness and open acknowledgment of the problem have led to increased interest and resultant explosion of knowledge in each of these areas. Research on this condition has produced many controversies, which also were expressed at this conference. Numerous questions were identified that may serve as foci for future research directions. These will depend on the development of precise agreement among investigators and clinicians in this field on the definition of what constitutes erectile dysfunction, and what factors in its multifaceted nature contribute to its expression. In addition, further investigation of these issues will require collaborative efforts of basic science investigators and clinicians from the spectrum of relevant disciplines and the rigorous application of appropriate research principles in designing studies to obtain further knowledge and to promote understanding of the various aspects of this condition.
Most of us are raised to believe that men are ravenous sex-beasts, eternally horny and only pretending to be a part of polite society so that they can find some new crevice to jam their Jeremy Irons into. So the first time we cross paths (and genitals) with a guy who can't get an erection, many of us immediately panic and assume that the problem must be us. We must be profoundly unsexy. After all, what could else possibly stop these hormone-addled maniacs from getting an erection?

Vardenafil and tadalafil belong to the same group of chemical compounds as sildenafil, namely phos-phodiesterase type 5 (PDE-5) inhibitors. Some men cannot benefit from sildenafil or the two newer PDE-5 inhibitors because they have low levels of nitric oxide. British investigators reported in late 2002 that three different types of compounds are being studied as possible medications for men with low levels of nitric oxide. They are Rho-kinase inhibitors, soluble guanylate cyclase activators, and nitric oxide-releasing PDE-5 inhibitors.

Erection is a vascular event. The penis becomes rigid when blood flow to the corpora cavernosa increases sixfold and venous outflow is physiologically impeded. Penile perfusion is governed by three organ systems—the neurologic, circulatory, and endocrinologic systems—each necessary for potency. The neurologic system accounts for vasodilation and venoconstriction of the corporal blood vessels so that blood is shunted to the erectile tissues; the circulatory system provides adequate blood flow to the hypogastric-cavernous bed, a distal branch off the internal iliac vessels; and the endocrine system, mediated by testosterone, plays a permissive role through mechanisms that have yet to be elucidated.
If you have been having ED for more than two months, you should see a doctor to find the cause. To detect the cause of ED, your doctor will take a history of when you started to have problems with erections and sex drive, illnesses or injuries that could cause ED, and any recent physical or emotional changes in your life. You also will need to review all the medications you take. The evaluation most often includes a physical exam.
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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
That means that as an adult, you need to activate the opposing parasympathetic system through sexually exciting visuals, thoughts and touches to get an erection going. But this nerve transmission is disrupted if you're stressed, anxious or distracted. The latter because you simply don't develop enough total stimulation of your genitals to get an erection, and the former because stress and anxiety all increase adrenaline – a key transmitter in the inhibiting sympathetic nervous system. They quite literally sabotage your erection.
#3 You’re not having enough sex. The more sex you’re having, the less likely you are to suffer from erectile issues. The American Journal of Medicine reports that men who had sex once *or more* a week were less likely to have issues getting and maintaining an erection. So, not having sex is actually one of the reasons you can’t get hard. [Read: 13 ways to have better sex and change the way you make love]

ED means no erections from masturbation. According to the American Urological Association, ED is “the inability to achieve or maintain an erection sufficient for satisfactory sexual performance.” Huh? That’s absurdly vague. If you define “an erection” as what you see in porn, and “satisfactory sexual performance” as porn sex—instant, hard-as-rock erections that last forever with climaxes always on cue—then just about every guy has ED. What is ED, really? For practical purposes, it means that a man who’s sober (no alcohol or other erection-impairing drugs) cannot raise even a semi-firm erection after extended masturbation.

Her remark was entirely destructive of poetry, since it was to the effect that poetry had nothing whatever to do with her; all her friends spent their lives in making up phrases, she said; all his feeling was an illusion, and next moment, as if to taunt him with his impotence, she had sunk into one of those dreamy states which took no account whatever of his existence.
early 15c., "physical weakness," also "poverty," from Middle French impotence "weakness," from Latin impotentia "lack of control or power," from impotentem (nominative impotens); see impotent. In reference to a want of (male) sexual potency, from c.1500. The figurative senses of the word in Latin were "violence, fury, unbridled passion." Related: Impotency.

Under normal circumstances, when a man is sexually stimulated, his brain sends a message down the spinal cord and into the nerves of the penis. The nerve endings in the penis release chemical messengers, called neurotransmitters, that signal the corpora cavernosa (the two spongy rods of tissue that span the length of the penis) to relax and fill with blood. As they expand, the corpora cavernosa close off other veins that would normally drain blood from the penis. As the penis becomes engorged with blood, it enlarges and stiffens, causing an erection. Problems with blood vessels, nerves, or tissues of the penis can interfere with an erection.
The observation that TRT enhances the efficacy of PDE5 inhibitors in hypogonadal men taking these therapies with suboptimal response to the PDE5 inhibitors alone has been reported.33 In addition, investigators have demonstrated that TRT in hypogonadal men can improve erectile function even without the benefit of PDE5 inhibitors.33 In addition, guidelines for managing ED in hypogonadal men by the European Association of Urology recommend controlling the man to a eugonadal state prior to initiation of PDE5 inhibitor therapy.36 Testosterone measurement consists of a serum specimen which should be ideally obtained in the morning because of the normal diurnal variation of testosterone which is at its peak in the morning. Since TRT is relatively safe, and men can potentially see an improvement in erectile function, it seems prudent to consider this issue when presented with a patient suffering from ED.
A system for inserting a pellet of alprostadil into the urethra is marketed as MUSE. The system uses a pre-filled applicator to deliver the pellet about an inch deep into the urethra at the tip of the penis. An erection will begin within 8 to 10 minutes and may last 30 to 60 minutes. The most common side effects of the preparation are aching in the penis, testicles, and area between the penis and rectum; warmth or burning sensation in the urethra; redness of the penis due to increased blood flow; and minor urethral bleeding or spotting.
Physical examination should include the assessment of male secondary sex characteristics, femoral and lower extremity pulses, and a focused neurologic examination including perianal sensation, anal sphincter tone, and bulbocavernosus reflex. More extensive neurologic tests, including dorsal nerve conduction latencies, evoked potential measurements, and corpora cavernosal electromyography lack normative (control) data and appear at this time to be of limited clinical value. Examination of the genitalia includes evaluation of testis size and consistency, palpation of the shaft of the penis to determine the presence of Peyronie's plaques, and a digital rectal examination of the prostate with assessment of anal sphincter tone.

Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.
Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.
The male erectile response is a vascular event initiated by neuronal action and maintained by a complex interplay between vascular and neurological events. In its most common form, it is initiated by a central nervous system event that integrates psychogenic stimuli (perception, desire, etc.) and controls the sympathetic and parasympathetic innervation of the penis. Sensory stimuli from the penis are important in continuing this process and in initiating a reflex arc that may cause erection under proper circumstances and may help to maintain erection during sexual activity.
Because of the difficulty in defining the clinical entity of erectile dysfunction, there have been a variety of entry criteria for patients in therapeutic trials. Similarly, the ability to assess efficacy of therapeutic interventions is impaired by the lack of clear and quantifiable criteria of erectile dysfunction. General considerations for treatment follow:

The most important organic causes of impotence are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this is somewhat less frequent but can often be helped. In psychological impotence, there is a strong response to placebo treatment.


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
If you have low blood pressure, heart disease, take medicines for heart disease or for high blood pressure, you shouldn’t use our service. If you take the medicines we prescribe you'll be at greater risk of serious side effects such as severe dizziness, fainting, heart attack, and stroke. Read the package insert that comes with the medicine for a full list of side effects and warnings.
The percentage of men who engage in some form of sexual activity decreases from 73% for men aged 57–64 years to 26% for men aged 75–85 years.3 For some men, this constitutes a problem, but for others it does not. The aetiology for this decline in sexual activity is multifactorial and is in part due to the fact that most of the female partners undergo menopause at 52 years of age with a significant decline in their libido and desire to engage in sexual activity. A study by Lindau and colleagues3 that examined sexuality in older Americans showed that 50% of the men in a probability sample of more than 3000 US adults reported at least one bothersome sexual problem and 33% had at least two such problems.3 This article will review the normal changes that occur with ageing, factors that influence these changes, individual variations and perspectives, and the available treatment options for ED and androgen deficiency.
Vardenafil and tadalafil belong to the same group of chemical compounds as sildenafil, namely phos-phodiesterase type 5 (PDE-5) inhibitors. Some men cannot benefit from sildenafil or the two newer PDE-5 inhibitors because they have low levels of nitric oxide. British investigators reported in late 2002 that three different types of compounds are being studied as possible medications for men with low levels of nitric oxide. They are Rho-kinase inhibitors, soluble guanylate cyclase activators, and nitric oxide-releasing PDE-5 inhibitors.
In the short term, alcohol relaxes muscles in the penis, letting blood to flow in (which is a good thing). However, alcohol also prevents other blood vessels from closing and trapping all the extra blood. Erections depend on trapping increased blood flow in the erectile tissue of the penis. If you don’t trap that extra blood, you don’t get an erection. In the long run, excessive alcohol consumption can cause liver scarring, high blood pressure, and can damage your blood vessels resulting in erectile dysfunction.
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