It is historically interesting that until the end of the 1970s erectile dysfunction was classified as predominantly psychogenic, although already Eckhard in 1863 and later v. Ebner had performed the first physiological investigations of the erection process [3, 4]. Unfortunately, these findings were forgotten for many decades. Only the possibility of inducing an artificial erection by injecting vasoactive substances was to change the basic anatomical and physiological understanding of the erection process and to question the previously held doctrine of an arterial shunt theory [2].
According to the original concept of Conti [2], erection initiation and its maintenance were controlled solely by an arterial blood shunt, according to which the detour of blood flow into the corpora cavernosa was made possible by the muscular cushions described by Ebner [3] in both the afferent and efferent legs of the penile vascular network. According to this concept, the cavernous cavities were considered to be merely passive blood reservoirs, which had to accommodate the increased blood inflow or the increased blood volume during erection caused by this.
Based on animal experimental studies, in the course of the 1980s the notion of erection genesis controlled solely by arterial inflow into “passive cavernous cavities” was revised in favor of active regulation by the smooth-muscular portions of the corpora cavernosa [5, 9, 10, 14, 15].
Experimental hemodynamic studies under pharmacostimulation finally confirmed that the erectile mechanism should be understood as a complex phenomenon based on arterial dilation, cavernous relaxation, and venous restriction [8,9,16]. Scanning electron microscopic studies of penile anatomy in humans and animals revealed for the first time a three-dimensional representation of erectile penile architecture in both erect and non-erect states [5,6].
Based on this work, a new concept of the erection mechanism could be derived, in which the relaxation of the smooth muscles of the corpus cavernosum plays a key role. According to current knowledge, the penile erection can be explained as follows:
Based on this expanded basic understanding, the anatomy, and physiology of penile erection can be described.
Contrary to several animal species, in humans the paired corpora cavernosa are directly connected by an incomplete septum (Fig. 4.1). Both corpora cavernosa are enveloped by the rigid tunica albuginea, resulting in complete separation of the corpus spongiosum, which lies below the corpora cavernosa, encases the urethra and is in direct anatomical relationship with the glans penis.
As shown in a schematic picture (Fig. 4.2), the two corpora cavernosa are supplied by the paired Aa. profundae penis, neuronally by innervation via the Nn. cavernosi. Between the so-called Buck's fascia and the tunica albuginea, the paired dorsal veins and nn. dorsales penis run laterally to the centrally located V. dorsalis penis profunda with its circumflex veins, all of which flow into the glans penis (see Fig. 4.2). The base of the penis is fixed to the symphysis and abdominal wall by a muscular ligamentous apparatus (Mm. ischiocavernosi and M. bulbospongiosus).
The vascular supply of the two corpora cavernosa runs primarily through the paired profundae penis with their corkscrew-like twisted tendril arterioles (helicinae). The glans penis is supplied by the two Aa. dorsales penis, which together take their origin from the Aa. pudenda interna. Only the corpora cavernosa provide rigidity during erection. They are constructed by a three-dimensional network of connective tissue and smooth muscle cells. In addition to the deep Vv. cavernosae at the base of the penis, a distal-subtunical venous plexus draining via circumflex veins provides venous outflow from the cavernous cavities.
In the non-erect state, the small arterioles opening into the sinusoidal cavities are tightly placed and twisted in a corkscrew-like fashion (Fig. 4.3). The corkscrew-like arrangement of the arterioles is what makes penile elongation possible in the first place, leading to stretching not only of the erectile tissues but also of the vascular structures of the corpus cavernosum muscles. The cavernous cavities communicate with each other via intersinusoidal cross-connections (see Fig. 4.3).
In addition to these functionally relevant arterioles, small nutritive capillaries are also found, with a maximum vessel diameter of 15 µm. The intersinusoidal connections existing between the cavernous cavities are significantly widened, which allows free communication between several sinusoidal spaces of the corpora cavernosa and thus makes the corpus cavernosa a functional unit (Fig. 4.5).
On the venous side, in the nonerect state, between the surface of the smooth corpus cavernosum muscles and the rigid tunica albuginea, there is a subtunical venous plexus located in the distal third of the penis with individual Vv. emissariae penetrating the tunica albuginea (Fig. 4.6). The cavernous cavities drained by the venous plexus are maximally contracted; the venous drainage network runs on their surface transverse to the covering tunica albuginea.
Whereas in the non-erect state the subtunically located venous plexus is fully exposed, under erection an entirely different picture emerges: Due to the massive relaxation of the smooth corpus cavernosum musculature with marked dilation of the sinusoidal cavities with consecutive blood filling, the special anatomical location of the subtunically located venous plexus results in compression of the smaller and larger intermediate venules (see Fig. 4.5), leading to venous occlusion. Only individual Vv. emissariae penetrating the tunica albuginea remain open and thus ensure continuous blood exchange in the penis, even in the fully erect state.
Based on our scanning electron microscopic studies, the erectile mechanism can be described as follows: while in the non-erect state the intracavernous profundae penis arterioles and their arterioles, as well as the cavernous cavities, are maximally contracted, the venous drainage network is maximally dilated, thus allowing free blood outflow via the emissary veins (Fig. 4-7). In contrast, during erection, there is dilation of the arterial vascular tree with consecutive increase in blood flow into the maximally relaxed and dilated sinusoidal spaces at the corpus cavernosum. The smallest venules located between the corpus cavernosum surface and the tunica albuginea are compressed between these two structures, resulting in venous restriction. Only single Vv. emissariae allow blood exchange even during a complete erection (Fig. 4.8).
Thus, the erection mechanism can be explained by 3 phenomena:
In contrast to the purely descriptive anatomy, the description of the physiological process of penile erection is much more difficult due to the essential neuropharmacological-physiological processes. From a purely physiological perspective, however, a clear picture of the erection mechanism can be shown, which can also be understood clinically, for example, by means of Doppler sonographic examinations on the patient.
In principle, two different types of erection are distinguished: psychogenic and reflexogenic erection. The former runs, among other things, via the sympathetic nerve cord and is not subject to the patient's will [1], the latter is purely reflexogenic and runs primarily at the spinal level [11].
The stimulating impulses are transmitted from the erectile center (S2-S4) via the cavernous nerve (Nn.erigentes) described by Eckhard [4] as early as 1864. As our own animal experiments have shown [11], the penile erection is initiated by the parasympathetically transmitted relaxation of the cavernous body muscles and the arterial dilatation.
The underlying mechanism at the cellular level is based on a release of acetylcholine from nerve terminals. Acetylcholine activates NO-synthase (NOS), which releases nitric oxide (NO) via a cascade of reaction sequences. Nitric oxide activates guanylate cyclase, which generates cyclic guanosyl monophosphate (cGMP) from guanosyl monophosphate (GMP). As a “second messenger,” cGMP causes intracellular relaxation of vascular and cavernous smooth muscle via a decrease in intracellular calcium levels. The degradation of cGMP and thus, ultimately, the termination of relaxation occurs via phosphodiesterases.
As a result, an intracavernosal pressure increase of 20 to 30 cmH2O below the systemic blood pressure is established (Fig. 4.9). The increase in intracavernosal blood volume and pressure results in compression of the subtunical venous plexus between the dilated sinusoidal cavities and the tunica albuginea. Maximum corpus cavernosum tumescence is achieved by this purely vascular mechanism controlled by the parasympathetic nervous system.
Only the compression of the tumescent corpus cavernosum by the Mm. ischiocavernosi induced shortly before orgasm leads to complete rigidity of the corpora cavernosa, with pressure values far above those of systemic blood pressure (> 400 mmHg). These results correlate with the findings of Lavoisier et al. [13], who demonstrated similar results regarding reflex contraction of the ischiocavernosi muscles and intracavernosal pressure increase in patients.
Contrary to original assumptions that detumescence is to be understood as a purely passive mechanism, it has been shown based on experimental studies [11] that stimulation of the sympathetically imprinted hypogastric plexus leads to detumescence of the corpora cavernosa, based on contraction of the smooth-muscle portions of the corpora cavernosa as well as the penile arteries (see Fig. 4.9). This mechanism can also be described as an inhibitory mechanism of erection.
In summary, a complete erection with maximal rigidity depends on the parasympathetic as well as the sympathetic and somatomotor nervous systems being intact. Whereas initiation and maintenance of erection are purely parasympathetic-vascular phenomena, maximal rigidity is achieved only by contraction of the somatomotor innervated ischiocavernosi muscles in the tumescent state. Detumescence and decay of erection are primarily a sympathetically controlled phenomenon that occurs due to smooth muscle contraction and can be described as an inhibitory mechanism.
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