Morning exercises can do more harm than good. As the scientists from the University of British Brunela in Midleseks established, early training, which many go without even having breakfast may increase the risk of infectious diseases. The fact is that when physical activity is high in the morning, the protective forces of an organism reduce. This pattern was noted by scientists who had conducted a study involving 14 volunteers from the number of professional swimmers.
In different days they were asked to conduct exercises at 6 am or 6 pm with the requested them not to smoke, not to use alcohol and not to have sex for 12 hours before. Before and after training the scientists collected saliva samples. It was found that evening after physical activity the level of hormone cortisol, which suppresses the immune system, was lower. Also, it was found that after the morning training the level of a type of antibody-protective immunoglobulins Class A- was considerably reduced.
This means that the risk of infection penetration in the body of athletes increases. The results of the study, according to the authors, refer to all athletes: as professionals, as well as amateurs.
Wednesday, November 14, 2007
Viagra
As you’ve probably heard, Viagra (Sildenafil) is used to treat impotence in men who either can’t have or can’t maintain erections. On the market since March 1998, it’s one of the most commercially successful drugs ever launched, with millions of prescriptions filled at a cost of more than $ 1 billion during the first year alone. It even has the blessing of the
Just as important, here’s what Viagra can’t do. It isn’t an aphrodisiac; it can’t get you aroused when you’re not interested. And it’s not a performance-enhancer. If you’re healthy, Viagra won’t give you a faster or harder erection or help you last longer. In fact, in healthy men it can even cause a painful, long-lasting erection (a condition called priapism) that may lead to impotence if it isn’t treated quickly.
Viagra works for about 70 to 85 percent of men with impotence caused by physical factors, such as damaged nerves (a frequent effect of diabetes), narrowed blood vessels (an effect of atherosclerosis), or side effects from medications. It can also help men whose impotence stems from anxiety or other psychological causes.
These are small, preliminary studies, however, and further research is needed to find out whether these results are reliable. In the meantime, you should only take Viagra according to your doctor’s instructions.
You usually swallow one tablet about an hour before sex. It takes an hour to take peak effect, though the waiting time can range from half an hour to two hours. The process doesn’t begin automatically, though — you still need to be aroused in order to have an erection. Viagra starts clearing out of the bloodstream about two hours after you take it, and it’s mostly gone after six hours or so.
Normally, this is what happens when a man is aroused: A chemical called cyclic GMP triggers a chain of reactions that end up relaxing the penis muscles and letting extra blood flow in (rigid muscles don’t cause the hardness of an erection; the extra blood does).
Viagra boosts the levels of cyclic GMP in the penis. It does this by preventing an enzyme (a protein involved in a biochemical reaction) called phosphodiesterase type 5, or PDE5, from breaking down cyclic GMP as fast as it usually does. The result: Cyclic GMP stays around longer, the muscles relax, and more blood flows in and stays in. The most serious side effect of Viagra results from a possible drug interaction. Taking Viagra while you’re on any drug that contains nitrates, such as a common type of heart medication called nitroglycerin (the same chemical as dynamite, sold under many brand names including Nitrostat, Transderm-Nitro, Nitrolingual, and Nitrogyn), can cause a sharp and sometimes fatal drop in blood pressure. Talk to your doctor or pharmacist to make sure Viagra won’t interact harmfully with anything else you’re taking.
Even if you’re not on nitroglycerin, Viagra’s new label advises doctors to use caution in prescribing the drug to anyone with a history of cardiovascular disease, including heart attack, stroke, angina, or high or low blood pressure. That’s because if you should ever suddenly need to take nitroglycerin, the chance of an interaction with Viagra could be too great to risk. To date, at least 130 men have died shortly after taking Viagra. In most cases they had heart attacks, although it isn’t clear whether those were caused by Viagra or by the excitement and exertion of having sex after a long break.
Other side effects are related to the way Viagra works in the body. The enzyme blocked by Viagra, PDE5, is also found in other parts of the body, among them the blood cells known as platelets and some muscles around blood vessels. The drug can disrupt the way blood cells and vessels normally function in certain areas, including the head, skin, and stomach — which might explain many of its commonly reported side effects, such as headache (reported by 16 percent of users), flushed skin (10 percent), and indigestion (7 percent).
Viagra blocks PDE5 very well, but it can also partly block a closely related enzyme, PDE6, which is found in the retina of the eye. That’s why about 3 percent of men on Viagra experience visual side effects, including bluish or blurry vision and sensitivity to light. In July 2005, the FDA issued an alert that a small number of men lost eyesight in one eye some time after taking Viagra, Cialis, or Levitra. Doctors don’t know whether the drugs caused the vision loss, but people with certain conditions — like heart disease, diabetes, hypertension — are at higher risk of developing the complication. Similarly, men with existing eye conditions — like retinitis pigmentosa, for example — may need to steer clear of the drug altogether to avoid eye damage.
Friday, September 14, 2007
Is Viagra still popular?
The new viagra gel for rubbing replaces the potency stimulating pills. It contains nitroglycerin, which is used for vascular expansion, as well as to stop heart attacks. As the gel has shown no side effects during the research, then it can be purchased without a prescription. Residents of the EU will soon be able to find the new gel from impotency in the drug stores.
Saturday, September 1, 2007
High level of carbon monoxide in a smoker’s blood is dangerous.
The high concentration of carbon monoxide (CO-Roman letters) in the atmosphere of the planet is one of the causes of so-called the greenhouse effect - not only formed during industrial or automotive engines operating, but with millions cigarette smokers. That is the conclusion reached by the organizers of the study, conducted under the auspices of the European Union in 27 countries.
Scientists of the continent in the measures of the European “Help” program, led by French professor of pulmonology Bertrand Dautzenberg, and called to help smokers understand the harm of smoking and to part with this evil, during the 18 months studied the content of CO in the air, exhaled by the smokers and people without this harmful habit. Over 200 thousand measurements of exhaled gas in the air were made, and it was found that almost all tobacco adherents had CO concentration twice higher than non-smokers, the report said.
Thus, the researchers conclude, the smokers not only poison their body, but make the “contribution” to the pollution of the environment the same as industry and transport.
Carbon monoxide is a colorless poison gas, lack of smell, that gives it the title of “invisible killer”. With increasing its concentration in the blood of a person the delivery of oxygen in the important organs, such as the heart and brain is blocked. Also large and small blood vessels can suffer, that can be a source of chronic cardiovascular disease.
Adalat - Nifedipine is a calcium ion influx inhibitor (calcium channel blocker or calcium ion antagonist).
The antianginal and antihypertensive actions of nifedipine are believed to be related to a specific cellular action of selectively inhibiting transmembrane influx of calcium ions into cardiac muscle and vascular smooth muscle. The contractile processes of these tissues are dependent upon the movement of extracellular calcium into the cells through specific ion channels.
Nifedipine selectively inhibits the transmembrane influx of calcium through the slow channel without affecting, to any significant degree, the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions available within the muscle cells and an inhibition of the contractile processes. Nifedipine does not alter total serum calcium.
The specific mechanisms by which nifedipine relieves angina and reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action.
Nifedipine dilates the main coronary arteries and coronary arterioles both in normal and ischemic regions resulting in an increase in blood flow and hence in myocardial oxygen delivery.
Nifedipine by its vasodilatory action on peripheral arterioles, reduces the total peripheral vascular resistance. This reduces the workload of the heart and thus reduces myocardial energy consumption and oxygen requirements which probably accounts for the effectiveness of nifedipine in chronic stable angina.
The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilation and subsequent reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.
The negative inotropic effect of nifedipine is usually not of major clinical significance because at therapeutic doses, nifedipine’s vasodilatory property evokes a baroreceptor mediated reflex tachycardia which tends to counterbalance this negative inotropic effect. Continued administration of nifedipine to hypertensive patients has shown no significant increase in heart rate.
Although nifedipine causes a slight depression of sinoatrial node function and AV conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine has had no tendency to prolong AV conduction or sinus node recovery time, or to slow sinus rate.
Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine.
More information
Scientists of the continent in the measures of the European “Help” program, led by French professor of pulmonology Bertrand Dautzenberg, and called to help smokers understand the harm of smoking and to part with this evil, during the 18 months studied the content of CO in the air, exhaled by the smokers and people without this harmful habit. Over 200 thousand measurements of exhaled gas in the air were made, and it was found that almost all tobacco adherents had CO concentration twice higher than non-smokers, the report said.
Thus, the researchers conclude, the smokers not only poison their body, but make the “contribution” to the pollution of the environment the same as industry and transport.
Carbon monoxide is a colorless poison gas, lack of smell, that gives it the title of “invisible killer”. With increasing its concentration in the blood of a person the delivery of oxygen in the important organs, such as the heart and brain is blocked. Also large and small blood vessels can suffer, that can be a source of chronic cardiovascular disease.
Adalat - Nifedipine is a calcium ion influx inhibitor (calcium channel blocker or calcium ion antagonist).
The antianginal and antihypertensive actions of nifedipine are believed to be related to a specific cellular action of selectively inhibiting transmembrane influx of calcium ions into cardiac muscle and vascular smooth muscle. The contractile processes of these tissues are dependent upon the movement of extracellular calcium into the cells through specific ion channels.
Nifedipine selectively inhibits the transmembrane influx of calcium through the slow channel without affecting, to any significant degree, the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions available within the muscle cells and an inhibition of the contractile processes. Nifedipine does not alter total serum calcium.
The specific mechanisms by which nifedipine relieves angina and reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action.
Nifedipine dilates the main coronary arteries and coronary arterioles both in normal and ischemic regions resulting in an increase in blood flow and hence in myocardial oxygen delivery.
Nifedipine by its vasodilatory action on peripheral arterioles, reduces the total peripheral vascular resistance. This reduces the workload of the heart and thus reduces myocardial energy consumption and oxygen requirements which probably accounts for the effectiveness of nifedipine in chronic stable angina.
The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilation and subsequent reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.
The negative inotropic effect of nifedipine is usually not of major clinical significance because at therapeutic doses, nifedipine’s vasodilatory property evokes a baroreceptor mediated reflex tachycardia which tends to counterbalance this negative inotropic effect. Continued administration of nifedipine to hypertensive patients has shown no significant increase in heart rate.
Although nifedipine causes a slight depression of sinoatrial node function and AV conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine has had no tendency to prolong AV conduction or sinus node recovery time, or to slow sinus rate.
Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine.
More information
Saturday, May 19, 2007
Levitra - Proper Use of This Medicine
Special patient directions come with levitra. Read the directions carefully earlier you start using vardenafil and each time you get a refill of your medicine . This medicine usually begins to work within 60 transactions after taking it. It continues to work for up to 4 hours. Stimulation is required for an erection. If you have any questions about the use and benefits of vardenafil ask your health care professional. Dosing-The dose of vardenafil will be different for different patients. Be your doctor’s orders or the directions on the label . The following information includes only the average doses of vardenafil. If your dose is different, do not change it unless your doctor tells you to do so. * For oral dosage form (tablets): For treatment of cavernous dysfunction: + Adults up to 65 years of age-10 mg as a single dosage no more than once a day, 1 hour before intimate activity. If needed, your mD may change your dose. + Adults 65 years of age and older-5 mg as a single dose no more than once a day, 1 hour before sexual intercourse. If needed, your doctor may change your dose. Storage-To store this medicine: * Keep out of the reach of children. * Do not store in the bathroom, near the kitchen sink, or in other damp places. Heat or moisture may causal agency the medicine to break down. * Keep the medical specialty from freezing. Do not refrigerate. * Do not stay fresh outdated medicine or medicine no longer needed. Ask your wellness care professional how you should dispose of any medicine you do not use. Be indisputable that any discarded medicine is out of the reach of children.
Friday, May 18, 2007
Kamagra
Proffering better and prolonged erections to men, kamagra basically is a generic form of Viagra and helps men in combating erectile dysfunction with ease. Belonging to the group of medicines that works to delay the functioning of enzymes called phosphodiesterases, it helps in attaining and maintaining erection for long. Phosphodiesterase enzymes work and affect the penis area. By controlling these enzymes, kamagra tries to minimize the impact of erectile dysfunction in men. It is a superlative quality product of Ajanta Pharma. Leaving aside the minor disparity in name, packaging, labeling, shape, color and flavor, there is no major difference between this generic and branded version. Both embrace the same composition of active ingredient called sildenafil citrate and effectively combat erectile dysfunction for the paragon sexual pleasure. But unlike the branded version, all these benefits are provided interestingly at a low cost by kamagra. When it comes to the main objective behind the formulation of this wonderful drug, erectile dysfunction is the keyword word kamagra is designed for. The other secondary purposes comprise: - Betterment of sexual performance - Upgradation of sexual desire and stamina. Kamagra should be duly consumed by mouth and at least 45 minutes before the sexual encounter for the better results. However while its intake, doctor’s supervision is essential. And your kamagra dosage must be determined on the basis of your medical history and conditions. Do not take kamagra more than once in a day as it could be unsafe. To experience superior results, there are few additional precautionary points that one should adhered to. They are: - Kamagra should be stored at room temperature of 25 degrees C in a compact container away from heat, light and moisture. - The intake of the drug must be prohibited if one has had allergic reaction to kamagra or its particular ingredient. - Its dosage should not be exceeded without prior consultation with the doctor. - Excessive consumption of alcohol also must be avoided. - Kamagra should not be applied in women and children.
Saturday, May 5, 2007
Food additives lead to cancer
Recently, the European Comission published the law about the interdiction of the use of food dye E-128 in food production.
In the course of the studies it was found that it could be detrimental to human health, causing cancer.
This dye is used typically for meat products with a minimum content of cubplot component in 6%, and meat for hamburgers with a minimum content of plant or grain component in 4%.
The ban will apply to the use of E128, as well as the import of products with its content.
However, according to the EU Commissioner for Agriculture, the precise list of products containing this component does not exist.
Adalat - Nifedipine is a calcium ion influx inhibitor (calcium channel blocker or calcium ion antagonist).
The antianginal and antihypertensive actions of nifedipine are believed to be related to a specific cellular action of selectively inhibiting transmembrane influx of calcium ions into cardiac muscle and vascular smooth muscle. The contractile processes of these tissues are dependent upon the movement of extracellular calcium into the cells through specific ion channels.
Nifedipine selectively inhibits the transmembrane influx of calcium through the slow channel without affecting, to any significant degree, the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions available within the muscle cells and an inhibition of the contractile processes. Nifedipine does not alter total serum calcium.
The specific mechanisms by which nifedipine relieves angina and reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action.
Nifedipine dilates the main coronary arteries and coronary arterioles both in normal and ischemic regions resulting in an increase in blood flow and hence in myocardial oxygen delivery.
Nifedipine by its vasodilatory action on peripheral arterioles, reduces the total peripheral vascular resistance. This reduces the workload of the heart and thus reduces myocardial energy consumption and oxygen requirements which probably accounts for the effectiveness of nifedipine in chronic stable angina.
The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilation and subsequent reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.
The negative inotropic effect of nifedipine is usually not of major clinical significance because at therapeutic doses, nifedipine’s vasodilatory property evokes a baroreceptor mediated reflex tachycardia which tends to counterbalance this negative inotropic effect. Continued administration of nifedipine to hypertensive patients has shown no significant increase in heart rate.
Although nifedipine causes a slight depression of sinoatrial node function and AV conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine has had no tendency to prolong AV conduction or sinus node recovery time, or to slow sinus rate.
Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine.
More information
In the course of the studies it was found that it could be detrimental to human health, causing cancer.
This dye is used typically for meat products with a minimum content of cubplot component in 6%, and meat for hamburgers with a minimum content of plant or grain component in 4%.
The ban will apply to the use of E128, as well as the import of products with its content.
However, according to the EU Commissioner for Agriculture, the precise list of products containing this component does not exist.
Adalat - Nifedipine is a calcium ion influx inhibitor (calcium channel blocker or calcium ion antagonist).
The antianginal and antihypertensive actions of nifedipine are believed to be related to a specific cellular action of selectively inhibiting transmembrane influx of calcium ions into cardiac muscle and vascular smooth muscle. The contractile processes of these tissues are dependent upon the movement of extracellular calcium into the cells through specific ion channels.
Nifedipine selectively inhibits the transmembrane influx of calcium through the slow channel without affecting, to any significant degree, the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions available within the muscle cells and an inhibition of the contractile processes. Nifedipine does not alter total serum calcium.
The specific mechanisms by which nifedipine relieves angina and reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action.
Nifedipine dilates the main coronary arteries and coronary arterioles both in normal and ischemic regions resulting in an increase in blood flow and hence in myocardial oxygen delivery.
Nifedipine by its vasodilatory action on peripheral arterioles, reduces the total peripheral vascular resistance. This reduces the workload of the heart and thus reduces myocardial energy consumption and oxygen requirements which probably accounts for the effectiveness of nifedipine in chronic stable angina.
The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilation and subsequent reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.
The negative inotropic effect of nifedipine is usually not of major clinical significance because at therapeutic doses, nifedipine’s vasodilatory property evokes a baroreceptor mediated reflex tachycardia which tends to counterbalance this negative inotropic effect. Continued administration of nifedipine to hypertensive patients has shown no significant increase in heart rate.
Although nifedipine causes a slight depression of sinoatrial node function and AV conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine has had no tendency to prolong AV conduction or sinus node recovery time, or to slow sinus rate.
Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine.
More information
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