Male health research: Investigating the impact of cavernous sinus pressure on circulatory return and health

The Influence of Cavernous Sinus Pressure on Penile Venous Return

During penile erection, the occlusion of penile veins plays a crucial role. Incomplete venous occlusion can lead to weak erections and premature ejaculation. Previous views held that penile venous occlusion during erection primarily relied on the contraction of the veins themselves and the closing of venous valves. Recent studies have shown that penile venous occlusion mainly depends on sufficient pressure within the cavernous sinuses. As shown in Figure 1, in the flaccid state, the cavernous sinus cavity is small, and the intersinus veins and subtunic veins are dilated, allowing for unimpeded blood return. In the erect state, the cavernous sinus cavity expands, increasing intracavitary pressure, compressing the intersinus and subtunic veins, interrupting blood flow, and achieving venous occlusion. Therefore, the relaxation of the smooth muscle cells of the corpus cavernosum and the cavernous sinuses plays a key role in maintaining penile erection. Pathological changes in these tissue structures caused by any reason can lead to erectile dysfunction.

Failure to fill the cavernous sinus artery is a common abnormality in patients with erectile dysfunction, caused by anatomical, cytological, and biochemical issues. For example, trauma causing communication between the corpora cavernosa and the corpus spongiosum can lead to penile venous fistula; Peyronie's disease can also cause incomplete closure of penile veins, primarily due to thickening of the tunica albuginea. However, the most important factor is the pathological changes in the smooth muscle cells and cavernous cavity of the corpora cavernosa, such as a decrease in the number of smooth muscle cells, cellular dysfunction caused by changes in cell ultrastructure, and extensive fibrous tissue proliferation. Without this underlying pathological change, penile venous fistula will not easily occur. This is because the failure of penile vein occlusion is not a simple hemodynamic result of rapid arterial blood loss. Normal penile erection occurs under the control and participation of the nervous system. When neurotransmitters in the blood bind to receptors on the surface of endothelial cells between the smooth muscle cells of the corpus cavernosum, these endothelial cells begin to produce nitric oxide (NO), which diffuses into adjacent smooth muscle cells. Through a series of chemical reactions, the smooth muscle cells relax, the cavernous sinuses expand, arterial blood flows into the sinus cavity, the intracavitary pressure increases, and the intersinus and subtunic veins are blocked, completing the erection process. Therefore, increasing the pressure within the cavernous sinuses is a key step in blocking venous blood flow to the penis to promote erection; once this step is impaired, venous occlusion failure is inevitable. In the past, clinical treatment of patients diagnosed with "venous fistula-related erectile dysfunction" using penile dorsal deep vein ligation often yielded unsatisfactory results. A significant factor contributing to this outcome was the failure to address the root cause of the venous fistula—insufficient pressure within the cavernous sinuses. Therefore, increasing penile arterial blood flow and raising the pressure within the cavernous sinuses is one of the effective measures for treating "venous erectile dysfunction."

We previously observed the corpora cavernosa of the penis in some patients with erectile dysfunction using scanning electron microscopy. The results showed that the loose structure in the corpora cavernosa of these patients disappeared, replaced by a large amount of proliferating collagen fibers (see Figures 3, 4, 5, 6). This proliferating fibrous tissue significantly weakens the compliance and elasticity of smooth muscle cells and the cavernous sinuses, severely restricting blood filling of the cavernous sinuses and the increase in intrasinus pressure. This pathological change can lead to two unfavorable consequences for penile erection:

① Reduced compliance and expansion function of the cavernous sinuses, insufficient arterial filling, and weak erection;

② Obstruction of penile arterial blood flow into the cavernous sinuses, preventing the intrasinus pressure from reaching the level required to occlude the veins, resulting in incomplete venous occlusion and rapid blood loss from the penile veins, leading to premature erection. These conditions are important factors contributing to weak erections and short duration of erection in clinical patients with erectile dysfunction. There are many clinical causes of erectile dysfunction, and the pathological changes in the corpora cavernosa of the penis caused by these various reasons are also different. To achieve satisfactory clinical treatment results, it is essential to identify the cause of erectile dysfunction and treat it accordingly. Otherwise, blindly taking Chinese or Western medicine without knowing the cause will hardly achieve the desired therapeutic effect. For patients with "refractory" erectile dysfunction who have not responded to various medications and methods, a comprehensive clinical examination should be performed, and a penile cavernosa biopsy should be performed if necessary. If the pathology confirms severe local pathological changes and general treatment cannot restore erectile function, penile prosthesis implantation surgery should be recommended.