niarceel wrote:
I used Viagra and Cialis for almost 10 years before their desirable effects began to fade. I have a great cardiovascular system (I was a runner for decades), normal blood pressure, no arterial plaque or deposits, in overall good health, so, I asked my doctor, "What could be the problem?"
His answer: "Venous leakage". He explained to me that our veins have tiny check valves in them to prevent the back flow of blood in our bodies during the heart's diastolic (resting) phase of a heartbeat. As we age, these tiny valves fray around the edges and start to leak, causing some back flow.
That back flow out of the penis is enough to interfere with/ruin an erection.
I was intrigued by your urologists possible explanation of the cause of venous leakage in your case.
His explanation of the degeneration of the valves in the veins of the penis facilitating venous leakage did not make complete sense to me. With all due respect, that theory does not hold up very well to others that I have researched.
Let’s take a closer look at erectile function:
Blood enters the penis via the cavernosal arteries. When in the flaccid state these arteries are constricted by tonic sympathetic influence. This lessens arterial inflow. The helicine arteries in the corpus cavernosum (CC) and the smooth muscle in the trabeculae amongst the sinusoidal spaces are also contracted by the same influence. The emissary veins on the outside of the corpora and the subtunical venous plexus are fully open(not compressed) so outflow is at full capacity. A minimal amount of blood is entering the penis and maximal outflow is permitted in this state.
Before we go further we need to understand that there are only valves in the veins leaving the penis, not in the arteries suppling the penis. There is however, something like a valve in the helicine arteries called “intimal cushions”, these are actually smooth muscle similar to what is in the trabeculae(structure of the corpus cavernosum). The helicine arteries are a complex network of smaller supply vessels the feed into each of the CC from the main cavernosal larger artery. There are many diagrams on the internet where you can sight all these elements in the penis if interested.
When tumesance begins from either tactile or mental stimuli, the various pathways involved (I won’t go into this) initiate relaxation of the smooth muscle in both the cavernosal arteries and the helicine arteries and the smooth muscle in the trabeculae. This allows a much greater in flow of blood into the penis. If relaxation is adequate in all three components, blood inflow is sufficient to cause the CC to expand greatly in size and stretch the tunica albuginea (TA). The veins that leave the CC pass just underneath and through the TA, are compressed during this process causing venous occlusion, out flow has been severely restricted. Inflow continues to be exaggerated due to the continued relaxation of the above mentioned vessels/structures.
Arteries generally do not need valves as pressure from the heart is usually strong enough to not cause back flow. Thus if the vessels into the penis are fully dilated from healthy amounts of active smooth muscle being relaxed, constriction of the emissary veins and the venous plexus leaving the CC will be optimal. Back flow from these veins is unlikely as they are in highly compressed state! Even if there was a small amount of backflow due to aging, it would not compromise the erectile process as in essence it would be further supplying the penis with blood from the other direction!
For an erection to fail there needs to be an avenue for the blood to escape from the penis via the vein network leaving the penis. It could do this in two ways, failure of relaxation of the above mentioned components involved with relaxation, or possible failure of the tunica albuginea itself to compress the veins that pass through it. I cannot see how the valves in the veins further down the track could be implicated in this. But if so I would like to know!
I have read many possible explanations, hypotheses on the causes of venous leakage, but not this one. I tried to search for this possible cause of ED and I found no published articles or studies on the subject.
I feel the following is a more likely scenario of what could be occurring. There has been a considerable amount of research into the loss of smooth muscle in the arteries and penile tissues due to the aging process. For venous occlusion to occur there needs to be sufficient relaxation of the supply vessels and the structure of the corpora cavernosa occurring for an erection to happen. If this is compromised by any of these possible aetiologies: sympathetic hyperactivity, endothelial dysfunction, oxidative damage, smooth muscle degeneration, fibrosis, atherosclerosis to the cavernosal arteries; pressure in the penile tissues will be insufficient to expand the CC to compress the veins close to and in the TT. We then have venous leakage, as blood can escape through the vein network. Much research has shown that smooth muscle can deteriorate and lessen with age and one of the main ways this happens is via oxidative damage. Research has also shown that this also occurs due to the loss of androgen's, in fact, it has been shown that penile health can be substantially compromised by the lack of androgens.
The other plausible suspect of venous leakage is as I mentioned above is the tunica albuginea, which may suffer from atrophy or a change in its structure so that it cannot compress the veins directly underneath as effectively as it once did. It is mainly composed of collagen and elastin. Studies have shown degenerative changes in specimens from some men suffering with venous occlusive dysfunction. Atrophy of the collagen fibres was seen, with their arrangement being irregularly orientated and the elastin fibres were scarce compared with controls. The integrity of the fibrous tissue of the TT appears to play a significant role in maintaining an erection.
There is also one other interesting possible cause of venous leakage and that is the formation of adipocytes (fat cells) in the subtunical region of the penis, which is directly adjacent to the CC. This is where the venous plexus veins lie and where the emissary veins leave the CC. Any change in structure in this section could affect the ability of the CC to compress these veins. It has been seen by research that these adipocytes form in this area due to possible androgen (testosterone) insufficiency and other causes such as oxidative stress and aging. Fat cells in this critical area could adversely affect venous occlusion.
The above makes sense to me.
It also makes sense that fraying or decay to the small valves in veins in the legs can cause varicose veins as blood has more of a tendency to pool rather than be pumped back to the heart.
The observations that have been made with regard to the loss of smooth muscle in the penile tissues and arteries would also help explain why the effectiveness of PDE5 inhibitors wane over time. PDE5 inhibitors work directly at helping the smooth muscle to relax. If the quantity and quality of smooth muscle is slowly decreasing it stands to reason that the effect of the inhibitors will also lessen. This does not take into account fibrosis and the deposition of collagen that also occurs with this loss of smooth muscle, which hinders penile elasticity and compliance. It also does not take into account the increase in sympathetic activity in the penile tissues as we age also. Both of which possibly contribute to venous leakage simply by not allowing the penis to expand enough to enable venous occlusion.