I am familiar with how Viagra and other dilators work, but I am not sure how it works with the prostate.
Couple of things, if he had a total TURP or not. As well, Viagra is NOT just a dilator as many assume since it is contraindicated with Nitrates.
I had to write an article on erectile dyfunction (ED), so here is some info on Viagra; I had on reference.
Forewarn it is lengthy but has a lot of information.. probably more than anyone would like to know, but it is medical and there is a
LOT of men that take it and refuse to tell EMS crews, and as well EMS crews forget to ask med.'s including Viagra.
VIAGRA® (sildenafil citrate)
Classification: Anti-impotence agent
Viagra® (sildenafil citrate) is a type 5 phosphodiesterase (PDE5) inhibitor, discovered and produced by drug company Pfizer, Inc. for the treatment of male erectile disfunction. Sildenafil citrate is an oral agent that works peripherally by enhancing the effect of nitric oxide on the smooth muscle of arteries and sinusoids of the corpora cavernosa.
Effective erection involves the release of nitric oxide (NO) by specialized nerves in the corpora cavernosa of the penis. NO activates the enzyme guanylate cyclase which thus increase the level of cyclic Guanosine Monophosphate (c-GMP) within the cells of the corpus cavernosum.
Metabolism
Viagra is absorbed into the blood between 30 and 120 minutes after ingestion, although high fat meals can decrease its absorption by 29%.
The drug is metabolized in the liver and excreted primarily in feces (80%).
In cases of overdose, dialysis does not significantly affect its excretion, since only 13% is excreted in the urine.
Viagra® interferes with the normal enzymatic breakdown of (c-GMP) by blocking the action of type 5 phosphodiesterase (PDE5). Type 5 phosphodiesterase is an enzyme that turns c-GMP into the inactive molecule GMP.
(cGMP) is a common intracellular molecule that is involved in many cell processes including: regulation of ion channels and smooth muscle relaxation. Blocking the enzymatic degradation of c-GMP in the corpus cavernosum results in prolonged smooth muscle relaxation, arterial dilation and improved engorgement.
Erectile dysfunction (ED) is the inability to sustain an erection sufficient for satisfying sexual activity. The Massachusetts Male Aging Study (MMAS) reported that 52% of participants, aged 40-70 years, had some degree of erectile difficulty. Other studies indicate that between 18 and 30 million American men are affected by ED.
Erection results when nerves in the corpora cavernosum are stimulated to release substances which cause the smooth muscle of the corpora cavernosa to relax. Relaxation of the vascular smooth muscle increases arterial blood flow into the sinusoids of the corpora cavernosa. Stimulation can be physical, psychological or both.
Causes:Erectile dysfunction can be caused by any of the following etiologies:
Psychogenic
Vasculogenic
Neurogenic
Endocrine
End-organ failure
Iatrogenic and drug induced
Psychogenic ED is now thought to account for less than 30% of cases. Psychogenic pathology can result in inhibition of the spinal erection center and/or excessive sympathetic stimulation. When sympathetic stimulation predominates, the smooth muscle of the corpora cavernosa can not fully relax.
Vasculogenic ED: may result from conditions which affect blood flow within the penis. Atherosclerosis, diabetic vasculopathy, hypertension, smoking, hyperlipidemia and trauma can diminish blood flow and erectile function.
Neurogenic ED: can result from lesions in the peripheral, spinal or cerebral nerves that serve the perineum and genitals. Diabetes, multiple sclerosis, tumors, disc herniation, Parkinson's, stroke, Huntington's chorea and electroshock therapy have all been associated with erectile dysfunction.
Endocrine & metabolic disorder ED: diabetes is the leading cause of ED in the US. Between 30 and 50% of all diabetic American men over 50 are impotent. Hypogonadism is the primary endocrinopathy causing ED. Hypogonadism can result from testicular failure to produce androgens or a failure of the anterior pituitary to produce luteinizing hormone. ED is also associated with: hyperprolactemia, thyroid disorders, uremia and dialysis (often reversible following kidney transplant).
End-organ failure: congenital defects, Peyronie's disease, priapism, prostatitis and seminal vasculitis have all been associated with ED.
Iatrogenic and drug induced ED: GU trauma related to surgery or irradiation and certain procedures performed on the spinal and brain can cause ED. Alcohol, sympathomimetics, antihypertensives, psychotropics and recreational drugs have all been associated with ED.
Until the discovery of Viagra, treatment options for ED included:
penile prosthesis
vacuum pump and occlusive bands
transurethral alprostadil
intracavernosal injections of vasoactive agents, such as alprostadil
CNS acting oral agents like yohimbe
Side Effects
Side Effects
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According to the manufacturer, there are three common side effects associated with Viagra:
headache (16%),
flushing (10%), and
dyspepsia (7%).
Other, less common, side effects include:
nasal congestion (4%),
transient vision changes (3%),
diarrhea (3%),
dizziness (2%), and
rash (2%).
Dyspepsia (17%) and abnormal vision (11%) occurred more frequently at the 100 mg dose.
Less than 2% of the 3700 patients tested had any cardiovascular side effects, although there is a degree of cardiac risk associated with sexual activity.
According to Lechtenberg and Ohl, men experience an elevation in blood pressure during sexual arousal. After arousal, during the plateau phase, hyperventilation, skeletal muscle tensing, and tachycardia (up to 175 beats/min) occur. Patients should be thoroughly examined by a physician for cardiac risks before taking Viagra to increase their sexual activity.
Viagra is also contraindicated for patients using organic nitrates such as nitroglycerine. Viagra potentiates the hypotensive effects of these drugs
Precautions
Precautions
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As already mentioned, patients should be assessed for cardiac risk before being prescribed Viagra. Viagra in combination with nitrates of any form can increase the risk of life threatening hypotension. The use of PDE-5 inhibitors like Viagra, Cialis and Levitra should be considered carefully in patients taking any anti-hypertensive medication.
The effect of
Viagra can be increased by enzyme inhibitors such as: cimetidine, erythromycin, ketoconazole and others. Patients need to be educated about the dangers of hypotension and prolonged erection.
Pfizer, Inc. also recommends that Viagra be used with caution in patients that have anatomical deformation of the penis and in patients who have conditions which may predispose them to priapism. Priapism is a persistent erection of the penis not associated with sexual arousal. In most cases, the arterial supply is excessive, the venous drainage is inadequate, or there is a combination of the two conditions (Lechtenberg and Ohl, 1994). Sickle cell anemia, leukemia, and multiple myeloma are conditions known to predispose patients to priapism
How it works
Pharmacodynamics
Orally administrated sildenafil citrate is rapidly absorbed and widely distributed in tissues. Onset occurs within one hour and has a duration of about four hours. It is mostly metabolized in the liver.
Viagra selectively inhibits the action of type 5 phosphodiesterase (PDE-5). PDE-5 is found in relatively high levels in corpora cavernosa. PDE-5 causes the enzymatic conversion of cGMP to the inactive molecule GMP. The longer cGMP is available to relax smooth muscle, blood flow into the erectile tissue can continue, increasing the potential for a sufficient erection.
Viagra only effects a man's ability to have and maintain an erection. It does not increase sexual interest. It is dependent upon physiological changes brought about by stimulation and arousal.
Sexual function in men includes several stages:
arousal,
erection,
orgasm,
ejaculation, and
fertility.
Normally sexual arousal occurs because of sexual thoughts and fantasies or direct stimulation. According to Guyton (1991), "...the male sexual act results from inherent reflex mechanisms integrated in the sacral and lumbar spinal cord, and these mechanisms can be initiated by either psychic stimulation or actual sexual stimulation but most likely a combination of both (p. 890)."
Parasympathetic impulses from the sacral portion of the spinal cord dilate the arteries of the penis. During stimulation, nitric oxide is released from postsynaptic nonadrenergic, noncholinergic neurons and also, but to a lesser degree, from endothelial cells. Ultimately, nitric oxide increases the number of cyclic guanosine monophosphate (cGMP) molecules in the cavernosal and arterial smooth muscle. The increase in cGMP results in the relaxation of smooth muscle. The relaxation of smooth muscle is crucial to reducing vascular resistance leading to engorgement and erection.
Now, all those years, you did not know it was so complexed huh?
