sildenafil-citrate and Arteriosclerosis

Atherosclerosis is a general health problem that not only affects the coronary arteries but also (in men) the penile arteries, thus contributing to organic causes of erectile dysfunction (ED) in heart disease patients. These organic causes are intertwined with psychological and pharmacological causes because medication prescribed for heart disease patients may also cause ED. The incidence of ED after myocardial infarction ranges from 38 to 78%. As sexual intercourse involves physical exertion, the medical history, ventricular function determined through echocardiography, and stress testing are used to classify patients into various groups where coital activity represents a greater or lesser cardiovascular risk. The energy requirements for intercourse are not high, ranging from 3.7 metabolic equivalents (METs) of energy expenditure at resting state during the preorgasmic phase to 5 METs during orgasm. The Bruce protocol for exercise stress testing is a six-stage protocol with changes in the slope and speed of the treadmill. As a general rule, a patient who completes the first two stages of the Bruce protocol has a functional capacity greater than 7 METs, which is considered sufficient for sexual intercourse. The physician or cardiologist concerned should institute first-line treatment with oral drugs according to the indications listed below. If sexual activity is not contraindicated, the treatment of choice for ED in heart disease patients is oral therapy with sildenafil, except in those cases in which its use is contraindicated. Specific recommendations are discussed.

Topics: Arteriosclerosis; Erectile Dysfunction; Heart Diseases; Humans; Male; Myocardial Infarction; Phosphodiesterase Inhibitors; Piperazines; Purines; Risk Factors; Sildenafil Citrate; Sulfones; Vasodilator Agents

Topics: 3',5'-Cyclic-GMP Phosphodiesterases; Adrenergic alpha-Antagonists; Arteriosclerosis; Blood Pressure; Carbolines; Contraindications; Coronary Disease; Cyclic GMP; Cyclic Nucleotide Phosphodiesterases, Type 5; Drug Interactions; Endothelium, Vascular; Erectile Dysfunction; Heart Rate; Humans; Hypotension; Imidazoles; Isosorbide Dinitrate; Male; Molecular Structure; Myocardial Infarction; Nitric Oxide Donors; Nitroglycerin; Phosphodiesterase Inhibitors; Phosphoric Diester Hydrolases; Piperazines; Purines; Randomized Controlled Trials as Topic; Sildenafil Citrate; Sulfones; Tadalafil; Triazines; Vardenafil Dihydrochloride; Vasodilation; Vasodilator Agents

Topics: Adult; Aged; Arteriosclerosis; Humans; Impotence, Vasculogenic; Male; Middle Aged; Piperazines; Purines; Sildenafil Citrate; Sulfones; Vascular Diseases; Vasodilator Agents

We studied the effect of chronic ischemia on prostatic smooth muscle contraction in the rabbit.. New Zealand male rabbits weighing 3 to 3.5 kg were assigned to 2 groups. Group 1 (10 rabbits) underwent balloon endothelial injury of the iliac arteries and received a 0.5% cholesterol diet for 4 weeks and then a regular diet for 8 weeks. Control group 2 (10 rabbits) received a regular diet. After 12 weeks the animals were anesthetized. Iliac artery and prostate blood flow was recorded. Prostate tissues were prepared for isometric tension measurement, enzyme immunoassay to determine cyclic guanosine monophosphate (cGMP) release and histological examination.. In group 1 atherosclerosis as well as a significant decrease in iliac artery and prostate blood flow were observed. Ischemia significantly increased prostatic tissue contraction, decreased cGMP release and led to capsular and stromal thickening, and epithelial atrophy. The alpha1-adrenoceptor blocker doxazosin and the phosphodiesterase-5 inhibitor sildenafil citrate significantly decreased the contraction of control and ischemic tissues. Doxazosin was more effective in decreasing contractions when it was combined with sildenafil or the nitric oxide (NO) precursor L-arginine. In contrast, doxazosin was less effective when it was combined with the NO synthase inhibitor N omega-nitro-L-arginine or with the guanylate cyclase inhibitor methylene blue. Doxazosin significantly increased cGMP release in control tissues but not in ischemic tissues. Sildenafil significantly increased cGMP release in control and ischemic tissues.. Ischemia increased prostatic smooth muscle contraction and led to marked structural damage. Stimulators of NO synthesis and cGMP production enhanced the efficacy of doxazosin in decreasing prostatic tissue contraction. Sildenafil decreased contractility and increased cGMP release. Increased smooth muscle tone and structural changes in the ischemic prostate may suggest a role for prostate ischemia in resistance to urinary flow independent of prostate size.

Topics: Adrenergic alpha-Antagonists; Animals; Arginine; Arteriosclerosis; Blood Flow Velocity; Cyclic GMP; Doxazosin; Electric Stimulation; Iliac Artery; In Vitro Techniques; Ischemia; Laser-Doppler Flowmetry; Male; Muscle Contraction; Muscle, Smooth; Nitric Oxide; Phosphodiesterase Inhibitors; Piperazines; Prostate; Purines; Rabbits; Sildenafil Citrate; Sulfones