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Vasculogenic Erectile Dysfunction

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Vasculogenic ED

Vasculogenic and Drug Induced ED

Erectile dysfunction (ED) is more frequent in patients with other signs of artherosclerotic disease such as ischaemic heart disease and arterial leg disease (20-22) and erectile dysfunction and cardiovascular disease share the same risk factors such as hypertension, diabetes mellitus, hypercholesterolemia and smoking (23,21).

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ED and presence of a flow limiting stenosis

Moreover, arterial lesions in the pudental arteries (penal erectile arteries) are much more common in men with ED than in the general population of a similar age. (24). Originally arterial disease was linked to ED by the French surgeon, Leriche in 1940. The cause for ED in such patients can be ascribed to the presence of a flow limiting stenosis (narrowing) caused by the artherosclerotic lesions, leading to a reduced blood flow to the corpus cavernosum (erectile tissue) during the erection process. This can lead to corporal veno-occlusive disorder (see below). Chronic ischaemia (oxygen deficiency) provoked by stenosis of the penile arteries is also associated with functional changes in the distal part of the penile vasculature such as decreased Nitric Oxide Synthase (NOS) activity and reduced endothelium dependent neurogenic NO-mediated relaxation in cavernosal tissue (25,26).

 

Two vascular factors are important in the onset of erection: adequate arterial inflow into the cavernosal arteries and an efficient veno-occlusive mechanism (trapping the blood inside the corpora cavernosa). Two types of vasculogenic ED can be theoretically distinguished:

  1. Arteriogenic - with reduced arterial inflow is the most frequent organic cause of ED (40-80% of all cases of organic ED). Arteriosclerosis is the most common cause of arterial disease. It is usually diffuse, but may be localized to vessels supplying the penis. Smoking, hyperlipidemia and diabetes are risk factors. Arteriogenic ED is much less commonly caused by Traumatic Injury of the penile arteries.

  2. Venogenic - with dysfunction of the veno-occlusive mechanism resulting in an excessive leakage of blood from the penis.

 

 

 

 

Reduced Arterial Inflow leads to ED via a complex Mechanism:

Reduced penile blood flow leads to a relative impairment of oxygenation (ischaemia) of cavernosal tissue leading to atrophy of smooth cavernosal muscle and fibrosis. The resulting 'non-use atrophy',and smooth muscle dysfunction in turn prevents adequate compression of the subtunical venules inside the tunica albuginea with a breakdown in the veno-occlusive mechanism. Venous leakage develops, resulting in decreased rigidity or absence of erection.

Various kinds of drugs can induce ED. The prevalence of this aetiology is difficult to assess, as the underlying condition treated by the drugs may also cause ED (arteriosclerosis, depression, anxiety, etc). Often such patients are taking multiple medications making it difficult to determine the contribution of a single drug. There is little evidence to suggest modifying drug treatment can restore erectile function (except for hormones inducing hypogonadism). However, it is worth trying in most cases, while maintaining effective treatment of the primary condition. Many modern drugs in the classes shown are not associated with sexual side-effects in placebo controlled studies. Ask your GP for further information.

 

 

 

Drugs and ED - probable mechanism:

  1. Antihypertensives - Decreased arterial blood flow to penis.
  2. Antiandrogens - influence testesterone levels
  3. Sedatives - Sedative effect
  4. Psychotropic Drugs - Action on central nervous system
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Vasculogenic and Drug Induced ED

Erectile dysfunction (ED) is more frequent in patients with other signs of artherosclerotic disease such as ischaemic heart disease and arterial leg disease (20-22) and erectile dysfunction and cardiovascular disease share the same risk factors such as hypertension, diabetes mellitus, hypercholesterolemia and smoking (23,21).

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References

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  • Huber N, Wood C, Babauan R, Madsen L, Shem Y, Wen S, Wang R. Recovering penile length and erectile function following radical prostatectomy. J Sex Med 2006;3(Suppl 1):21 (Abstract 60).
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  • J Urol, 159: 2229-2236, 1998. McCulloch DK, Campbell IW, Wu FC, Prescott RJ, Clarke BF. The prevalence of diabetic impotence. Diabetologia, 18:279-283, 1980. Mcculloch DK, Young RJ, Prescott RJ, Campbell IW, Clarke BF. The natural history of impotence in diabetic men. Diabelogia, 26: 437-440, 1984.
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  • Saenz De Tejada I, Goldstein I, Azadzoi K, Krane RJ, Cohen RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med, 320: 1025-1030, 1989.
  • Pickard RS, King P, Zar MA, Powell PH. Corpus cavernosal relaxation in impotent men. Br J Urol, 74: 485-491, 1994. Pickard RS, Powell PH, Zar MA. Nitric Oxide and cyclic GMP formation following relaxant nerve stimulaton in isolated human corporus cavernosum.
  • Br J Urol, 75: 516-522, 1995. Seftel AD, Vazin ND, Ni Z, Razmjouei K, Fogarty J, Hampel N, Polak J, Wang RZ. Advanced Glycation end products in human penis: elevation in diabetic tissue, site of deposition and possible effect through iNOS and eNOS. Urology, 50: 1016-1026, 1997.
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  • Martin-Morales A, Sanchez-Cruz JJ, Saenz de Tejada I, Rodriguez R, Prevalence and independent risk for ED in Spain: results of the Epidemiologia de la Disfuncion Erectil Masculina Study. J Urol, 166: 569-574, 2001
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