Night erection - prevention of impotence

Nocturnal erections are usually attributed to erotic dreams, a full bladder, or high testosterone concentrations at this time of day. However, the presence of this phenomenon in boys from birth disproves all these versions at once. An alternative hypothesis suggests that nocturnal erection is not a side effect of anything, but a targeted prevention of hypoxia in the tissues of the penis.

Why hypoxia is characteristic of the penis, how it is associated with age-related erectile dysfunction and how to maintain potency until old age, read about this in my new article.

Anatomy of the Penis The penis is sometimes jokingly called a muscle and there is some truth in this joke. This organ contains a huge number of smooth muscle cells (SMCs), which are the functional basis of the walls of the arteries and sinuses of the cavernous (cavernous) body. The blood filling of the corpus cavernosum depends on the tone of the SMC, and superficial (enveloping) veins with thin walls without SMC are responsible for blood diversion. These veins are located between the elastic corpus cavernosum and the rigid membrane with limited stretching, which is important for the implementation of the mechanism of a strong erection.

Mechanism of erection From the point of view of biomechanics, an erection is in a simple two-step process. At the first stage, as a result of relaxation of the SMC, the lumen of the cavernous arteries and sinuses increases, and under the pressure of the incoming blood, the corpora cavernosa expands. At the same time, the penis swells, but this is still not enough to straighten and stiffen it.

The fact is that the blood arriving in the cavernous sinuses is constantly discharged through the circumflex veins. However, with maximum relaxation of the MMC, the incoming blood expands the elastic corpus cavernosum to such an extent that it begins to press the veins against the hard shell of the penis. As a result of cross-clamping of the veins, the discharge of blood from the cavernous sinuses is blocked, therefore, the blood arriving through the arteries is trapped. This is the second stage in the development of erection, as a result of which the penis reaches its maximum size and rigidity sufficient for intercourse. So, an erection develops as a result of the expansion of the arteries bringing blood and the subsequent clamping of the veins. Ok, everything is clear with the vein clamping mechanism, but how is the tone of the SMC arteries regulated?

Regulation of erection At rest, sympathetic nerve fibers keep the MMC in good shape, so the penis is sluggish. An even stronger tone of SMCs develops when the surface of the body is cooled, which is familiar to every man in the form of a significant decrease in the size of the penis, for example, when swimming in cold water. There is nothing extraordinary in this, in a similar way the whole body reacts to cold; blood is redistributed to the center of the body from the skin, mucous membranes and all extremities (fingers, nose, penis) to reduce heat loss and prevent general hypothermia. However, even despite the cold, this ancient and important reflex is suppressed by the more dominant sexual one.

An erection develops on a command from the central nervous system (visualization or fantasy) and as a result of mechanical stimulation of the erogenous zones. Both signals intersect at the level of the lowest segments of the spinal cord, from where parasympathetic nerve fibers exit, transmitting the summed signal to the penis. In the nerve endings of these fibers, nitric oxide (NO) is synthesized from the amino acid arginine, which penetrates into the smooth muscle fiber of the arteries. Here NO activates an enzyme that converts the GTP nucleotide into cGMP, the accumulation of which causes the relaxation of the SMC of the cavernous arteries and sinuses and their filling with blood.

After orgasm, NO production stops, and cGMP is converted back to GTP. A decrease in the concentration of cGMP allows the sympathetic nervous system to dominate again to restore the tone of the SMC and thereby reduce blood flow and suppress an erection.

Thus, during the period of sexual arousal, the MMC are relaxed, which allows us to consider an erection a passive process. On the contrary, the calm state of the penis, from the point of view of the physiology of the MMC, is an active process that requires energy and oxygen. This factor plays a role in decreasing the strength of an erection with age.

Age-related erectile dysfunction The maximum strength of erection develops in men after puberty and then gradually decreases. In general, by the age of 40, 40% of men will face signs of age-related erectile dysfunction (EED), and an additional 10 years of life increases their share by 10%. A characteristic sign of foreign economic activity is the insufficient development of the second stage of erection in the presence of the first. That is, sexual arousal consistently causes swelling of the penis, but the proper rigidity is achieved only for a short time or is not observed at all. To understand the cause of this problem, let us analyze the pathogenesis of foreign economic activity sequentially at different anatomical levels: organ, tissue and cellular.

At the organ level, it is found that the incoming blood is constantly discharged through the outflow veins due to insufficient compression of their lumen from the corpus cavernosum. The fact is that with age, the corpus cavernosum gradually loses its ability to stretch and, with an erection, does not reach a size sufficient to press the veins against the outer shell of the penis. Therefore, increasing blood flow, even with the help of drugs, does not always solve the problem.

At the tissue level, a decrease in the elasticity of the corpus cavernosum is due to fibrosis and an increase in the number of collagen fibers in its tissues. Similar changes are typical for other tissues and organs with a deficiency of blood supply against a background of high oxygen demand (for example, with myocardial infarction). But what kind of deficiency of blood supply and lack of oxygen can we talk about in the penis?

At the cellular level, we find that oxygen deficiency (hypoxia) is due to the physiology of the MMC. Above, I have already mentioned that under conditions of sexual rest, MMC are in good shape almost around the clock, which reduces blood flow and the availability of oxygen to the surrounding tissues. Moreover, when performing the work, SMCs increase their own consumption of already deficient oxygen, causing even greater hypoxia in the tissues of the corpus cavernosum. Thus, the MMC literally saws the branch on which they sit and die from hypoxia themselves and grab all the cells that are voracious to oxygen into the next world. Without timely regeneration, the niches of dead SMCs and tissues of the corpus cavernosum are gradually occupied by more economical cells and collagen. These tissues do not need an abundance of oxygen, but they are unable to regulate blood flow and irreversibly reduce the elasticity of the corpus cavernosum, which is the basis for the development of VED.

After these lines, the smart reader will decide that the prevention of foreign economic activity can be provided with the help of hands, porn and Viagra. But things are not as simple as they seem.

VED therapy In 1992, the pharmaceutical company Pfizer prematurely curtailed clinical trials of a drug that was ineffective for increasing blood flow in the heart muscle in patients with angina pectoris. However, male study participants refused to return the remaining pills due to the attractive side effect of the drug increasing blood flow to another organ of love. Pfizer called her unsuccessful invention Viagra, adding the words vigor (strength) and Niagara (waterfall in America). Since then, a lot of money and the attention of researchers have made it possible to advance in the treatment and prevention of foreign economic activity.

Sildenafil (the active ingredient of Viagra) blocks the reverse reaction of the transformation of GTP into cGMP, causing the accumulation of the latter and the complete relaxation of the MMC. This makes it possible to implement the second stage of the erection mechanism, provided that the tissues of the corpus cavernosum are still sufficiently elastic and at least part of the SMC is viable.

At first glance, sildenafil does not affect the root cause of VED and improves erection only during the period of use of the drug. However, studies have shown that regular use of sildenafil increases the amount of HMC in the corpus cavernosum and has a positive effect on erection even after stopping treatment. Regular use of sildenafil improves the blood supply to the penis, providing oxygen and testosterone, and this promotes the regeneration of the MMC and the tissues of the corpus cavernosum.

From these results, the conclusion suggests itself that the problem can be solved by higher sexual activity or regular masturbation. But for some reason, in practice, such preventive training in erection does not give long-term results. Even a negative effect is possible, because a full erection blocks blood in the penis, which can aggravate hypoxia. For example, prolonged erection that persists after orgasm (priapism) can cause tissue necrosis, and in such cases, an urgent need to see a doctor for its relief. In addition, a deliberately induced erection is not always accompanied by high concentrations of testosterone in the blood, which will also not promote regeneration. Nevertheless, further studies of this problem led to the conclusion that preventive training in erection does take place, but occurs at night, when the regenerative processes are accelerating.

The role of nocturnal erection in the prevention of VED Once a nocturnal erection was considered the result of erotic dreams, but then the spontaneous nature of this phenomenon was established in an erection often occurs without appropriate plots of dreams and sometimes outside the phase of REM sleep. Later, they began to believe that nocturnal erection is just a side effect of increasing testosterone synthesis, the daily rhythm of concentration of which has a maximum at 3-6 a.m.