Effects of smoking on the reproductive system of man
The reproductive tract could not be left untouched by the action of harmful toxic substances released by smoking blood. In the last decade more and more publications referred to the negative effects on potential pregnancy and completion. About 30% of women in reproductive age and 35% of men smoke. From these groups only 22% aware of the harmful effects of tobacco on fertility. Men born to mothers who smoked had low sperm density, due to a possible concentration of cadmium ions and
nicotine derivatives in follicular fluid environment. Smoking is cited as gonadotoxic habit, which is responsible for the deteriorating production of low mobility of sperm in chronic smokers, and altering the morphology of spermatozoa. Chronic exposure to nicotine and tobacco can affect the sperm on the fertilization ability of the egg. A team of researchers in New York examined the ability pollinated men who smoked more than four cigarettes a day for 2 years or more. The insemination at 66% capacity of the samples of these men was negative. While only 28% of non-smoking failed fertilization test.From the group of heavy smokers (19 cigarettes per day), only 18% achieved the test, while the group of light smokers achieved in tests by 71%. The explanation given is that sperm carrying a nicotinic cholinergic receptor, which with time loaded with nicotine, thus slowing down the approach and adhesion of sperm to the oocyte plasma membrane. The DNA of gonadal cells plays an important role in fertility and the development and completion of fertilization. The change in DNA caused endorchikous, environmental, idiopathic and genetic factors. Environmental factors include elevated temperature of the testes from local infections, hormones, chemotherapy and smoking.
In infertile men the most common anatomical finding is varicocele (dilation of venous vessels around the testicle). The semen analysis in smokers with varicocele showed 25% reduction in the concentration of spermatozoa, 15% reduction of the mobility of spermatozoa and 17% reduction of the normal forms of spermatozoa. In the same study observed in smokers increased leucocytes in semen by 48%. This was interpreted as a response to inflammatory activity were topically inhaled smoke toxins, such as nicotine, carbon monoxide, cadmium and other mutagenic components of tobacco. A second interpretation given was that the aggregation of leukocytes is an indication of phagocytosis of abnormal sperm, produced under the influence of the above toxins.
To summarize, the male smokers present in semen analysis low sperm count, low sperm motility and growth of pathological forms of spermatozoa.
The effects of cigarette smoking are well known and scientifically documented in almost all organ systems of the human body. The effect of smoking on erectile function nowadays is researched. In Great Britain more than 120,000 men 30-40 years show total erectile impotence.
Erectile function is neurovascular which is controlled by the nitrogen oxide. The sequence of events that occurs aims to increase the supply of blood to the corpora cavernosa and simultaneously trap the blood in them with the relaxation of the muscle cells of the spiral arteries.
The activation of the cholinergic nerve endings in the penis becomes neurotransmitters acetylcholine, and nitric oxide, resulting in the signal is given for the relaxation of smooth muscle of the corpora cavernosa. The endothelial cells of the penile blood vessels produce nitric oxide, which is the primary neurotransmitter that controls operation of the erection. The production of nitric oxide is made by the action of the enzyme eNOS L Arginine.
Free radicals and aromatic components decrease endothelial synthesis of nitric oxide, acting in eNOS enzyme. Nicotine and other derivatives affect the production of nitric oxide from L Arginine. A peroxide antagonizes the oxide consistently contraction (instead of relaxation) smooth muscle. Nicotine also gives brain stimuli that lead to contraction of the penile tissue (vasospasm symptom) inhibiting the blood from entering the corpora cavernosa.
Several investigators have shown that smoking was more common in the erectile dysfunction clinic patients than in the general population. also showed that smoking and atherosclerotic disease were predisposing factors for organic erectile dysfunction. Smoking high-nicotine cigarettes reduces the vasodilation of the penile arteries. Smoking, another is independent factor in atherosclerotic blood vessels of the pelvis and to the penile arteries young erectile impotence.
The atheromatous disease is the most serious damage caused by smoking in the vessels. Smoking documented is an independent risk factor for atherosclerosis, equivalent to hypertension and hypercholesterolemia. However, atherosclerosis is a powerful cause of erectile failure and the need for taking medication for hypertension and hypercholesterolemia leads to erectile dysfunction medication because of adverse drug reactions.
The damage caused by smoking both on male fertility and erectile function, is proportional to the time the report of the body to toxic derivatives of tobacco, as well as their concentration. Chronic exposure of genital tissue to these toxic derivatives involves the risk of permanent and irreversible damage. It was observed that the prevalence of erectile dysfunction in former smokers was lower in current smokers. In the case of infertile men smoking cessation brought low by a sufficient degree of improvement in sperm parameters. The advice and referral to specialist smoking cessation in the therapeutic approach of these patients remains a top choice.
The reproductive tract could not be left untouched by the action of harmful toxic substances released by smoking blood. In the last decade more and more publications referred to the negative effects on potential pregnancy and completion. About 30% of women in reproductive age and 35% of men smoke. From these groups only 22% aware of the harmful effects of tobacco on fertility. Men born to mothers who smoked had low sperm density, due to a possible concentration of cadmium ions and
nicotine derivatives in follicular fluid environment. Smoking is cited as gonadotoxic habit, which is responsible for the deteriorating production of low mobility of sperm in chronic smokers, and altering the morphology of spermatozoa. Chronic exposure to nicotine and tobacco can affect the sperm on the fertilization ability of the egg. A team of researchers in New York examined the ability pollinated men who smoked more than four cigarettes a day for 2 years or more. The insemination at 66% capacity of the samples of these men was negative. While only 28% of non-smoking failed fertilization test.From the group of heavy smokers (19 cigarettes per day), only 18% achieved the test, while the group of light smokers achieved in tests by 71%. The explanation given is that sperm carrying a nicotinic cholinergic receptor, which with time loaded with nicotine, thus slowing down the approach and adhesion of sperm to the oocyte plasma membrane. The DNA of gonadal cells plays an important role in fertility and the development and completion of fertilization. The change in DNA caused endorchikous, environmental, idiopathic and genetic factors. Environmental factors include elevated temperature of the testes from local infections, hormones, chemotherapy and smoking.
To summarize, the male smokers present in semen analysis low sperm count, low sperm motility and growth of pathological forms of spermatozoa.
The effects of cigarette smoking are well known and scientifically documented in almost all organ systems of the human body. The effect of smoking on erectile function nowadays is researched. In Great Britain more than 120,000 men 30-40 years show total erectile impotence.
Erectile function is neurovascular which is controlled by the nitrogen oxide. The sequence of events that occurs aims to increase the supply of blood to the corpora cavernosa and simultaneously trap the blood in them with the relaxation of the muscle cells of the spiral arteries.
The activation of the cholinergic nerve endings in the penis becomes neurotransmitters acetylcholine, and nitric oxide, resulting in the signal is given for the relaxation of smooth muscle of the corpora cavernosa. The endothelial cells of the penile blood vessels produce nitric oxide, which is the primary neurotransmitter that controls operation of the erection. The production of nitric oxide is made by the action of the enzyme eNOS L Arginine.
Free radicals and aromatic components decrease endothelial synthesis of nitric oxide, acting in eNOS enzyme. Nicotine and other derivatives affect the production of nitric oxide from L Arginine. A peroxide antagonizes the oxide consistently contraction (instead of relaxation) smooth muscle. Nicotine also gives brain stimuli that lead to contraction of the penile tissue (vasospasm symptom) inhibiting the blood from entering the corpora cavernosa.
Several investigators have shown that smoking was more common in the erectile dysfunction clinic patients than in the general population. also showed that smoking and atherosclerotic disease were predisposing factors for organic erectile dysfunction. Smoking high-nicotine cigarettes reduces the vasodilation of the penile arteries. Smoking, another is independent factor in atherosclerotic blood vessels of the pelvis and to the penile arteries young erectile impotence.
The damage caused by smoking both on male fertility and erectile function, is proportional to the time the report of the body to toxic derivatives of tobacco, as well as their concentration. Chronic exposure of genital tissue to these toxic derivatives involves the risk of permanent and irreversible damage. It was observed that the prevalence of erectile dysfunction in former smokers was lower in current smokers. In the case of infertile men smoking cessation brought low by a sufficient degree of improvement in sperm parameters. The advice and referral to specialist smoking cessation in the therapeutic approach of these patients remains a top choice.
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