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From the * Department of Surgery and Experimental
Research, Faculty of Medicine, Cairo University, Egypt; and the
Department of Surgery, Faculty of Medicine,
Menoufia University, Shebin El-Kom, Egypt.
| Correspondence to: Ahmed Shafik, MD, 2 Talaat Harb Street, Cairo 11121, Egypt (e-mail: shafik{at}ahmedshafik.com). |
| Received for publication December 27, 2005; accepted for publication May 22, 2006. |
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Abstract |
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Key words: Ischio-/bulbo-cavernosus muscle, corpora cavernosa, intracorporal pressure, electromyography
The penile bulb is surrounded by the BCM, the penile crura and proximal part of the shaft by the ICM (Skandalakis et al, 2004). The BCM arises from the perineal body, and its anterior fibers end in a tendinous expansion which extends over the dorsal aspect of the penis covering the dorsal vessels (Skandalakis et al, 2004). The BCM assists in penile erection by compressing the erectile tissue of the penile bulb and the deep dorsal vein of the penis (Breza et al, 1989; Skandalakis et al, 2004). The ICM arises from the ischial tuberosity and ramus, and its fleshy fibers end in an aponeurosis attached to the sides and undersurface of the crus penis (Skandalakis et al, 2004).
The ICM and BCM are striated muscles and controlled by somatic nerves (Breza et al, 1989; Skandalakis et al, 2004). During the rigid erection phase, the flow in the internal pudendal artery is almost zero and in the cavernous artery is not measurable (Lue et al, 1988; Breza et al, 1989). The ICM and BCM come into action in the rigid erection phase, leading to suprasystolic ICP rise. The suprasystolic pressure is momentary and is transiently achieved during pelvic thrusting. It is not known whether the cavernosus muscles' contraction during the rigid erection phase is induced voluntarily or reflexly.
We hypothesized that cavernosus muscle contraction during the rigid erectile phase is reflexogenic, although the 2 cavernosus muscles are striated. This hypothesis was investigated in the current study.
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Materials and Methods |
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Methods
Erection was induced by intracavernosal injection of alprostadil
(Lue and Broderick 1998), while
the ICP and cavernosus muscles' electromyography (EMG) were being recorded.
The effect of cavernosus muscle contraction on the ICP was registered.
Cavernosus muscle contraction was induced voluntarily and by using electrical
stimulation. The ICP was measured by means of a 28-gauge needle inserted into
the corpus cavernosum (CC) at the middle of the penile shaft. The needle was
connected to a strain gauge pressure transducer (Statham 230B, Oxnard, Calif)
and via amplifiers to a chart recorder (Hewlett-Packard 7798A, Waltham,
Mass).
The EMG activity of the BCM and ICM was recorded by means of an EMG concentric needle electrode (type 13L49, DISA, Copenhagen, Denmark) measuring 45 mm in length and 0.65 mm in diameter, introduced into the ischio-cavernosus muscle; the ischial ramus with the overlying crus penis was palpated and the needle inserted into the medial aspect of the ramus. A second identical needle was placed in the bulbocavernosus muscle; the bulb of the penis was palpated and the needle electrode introduced into the muscle overlying it. A ground electrode was applied to the thigh.
The EMG activity was displayed on the oscilloscope of a standard EMG apparatus (Type MES, Medelec, Woking, UK). Films of the potentials were taken on light-sensitive paper (Linagraph type 1895, Kodak), from which measurements of the latency of the reflex and motor unit action potentials were made. The EMG signals were, in addition, stored on an FM tape recorder (Type 7758A, Hewlett-Packard, Waltham, Mass) for further analysis as required.
The correct position of each needle in the musculature was monitored by the burst of activity heard from the loudspeaker and visualized on the oscilloscopic screen as the muscle was entered. The normality of the myoelectric activity of the 2 cavernosus muscles was tested in all subjects prior to performing the experiment. This was done through muscle stimulation by means of a needle electrode introduced into the relevant muscle and recording the motor unit action potentials by the recording needle electrode. All the subjects had normal EMG activity of the cavernosus muscles. Fine adjustments of the needle position were made while the EMG reponse to needle insertion was observed on the chart recorder. Multiple recordings were done to assure reproducibility.
The ICM and BCM were either electrically stimulated or voluntarily contracted, and the corporal response was recorded in the flaccid and erectile phases. Cavernosus muscle stimulation was effected by a repeated series of 10 electrical stimuli of 200 ms duration at a frequency of 0.2 Hz and intensities between 0 and 100 mA. Alprostadil was then injected into the CC and the responses of the ICP, the BCM, and the ICM during the different stages of erection were recorded.
Corpora Cavernosa and Cavernosus Muscle Anesthetization
To test whether the cavernosus muscles' response to ICP elevation was
direct or reflex, the 2 cavernosus muscles were anesthetized while the penis
was in the rigid erection phase and the 2 muscles were contracting. The muscle
anesthetization was effected by injecting 2 ml of 1% lidocaine into the muscle
bundles around the electrode. The response of the ICP to lidocaine injection
of the cavernosus muscles was recorded after 10 minutes of lidocaine
injection. The test was repeated by infiltrating the cavernosus muscles with
normal saline.
On a different day, the CC was anesthetized; the penis was rubbed with lidocaine gel while in the rigid erection phase and while the cavernous muscles were recording increased EMG activity. The ICP response to penile lidocaine rubbing was recorded 10 minutes after lidocaine application. The test was repeated using bland gel instead of lidocaine gel.
To ensure reproducibility of the results, the tests were repeated at least twice in the individual subject, and the mean value was calculated. The results were analyzed statistically using the Student's t test, and values were given as the mean±SD. Significance was ascribed to P < .05.
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Results |
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The BCM and ICM EMG exhibited no resting electric activity. The intracorporal pressure in the flaccid phase recorded a mean of 10.6±1.2 cm H2O (range 9–12). On cavernosus muscle stimulation with the aforementioned parameters, they contracted, recording a mean amplitude of motor unit action potentials (MUAPs) of 292.3±39.7 µV (range 216–367) for the ICM (Figure 1) and of 264.5±32.8 µV (range 186–319) for the BCM (Figure 2). During ICM and BCM stimulation, the ICP did not exhibit a significant change against the basal pressure (P > .05) (Figure 3), and the penis remained flaccid.
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Response of the Cavernosus Muscles to Corpus Cavernosum Anesthetization
When the penis was rubbed with lidocaine gel while in the rigid erection
phase (mean intracavernosal pressure 142.6±10.2 cm H2O,
range 130–156) and with the cavernosus muscles exhibiting increased EMG
activity, the muscles' myoelectric activity disappeared and the ICP dropped to
a mean of 73.6±8.3 cm H2O (range 62–84). Repetition of
the test using bland gel instead of lidocaine did not affect the cavernosus
muscles' EMG activity. With the 2 cavernosus muscles exhibiting increased EMG
activity and the penis in the rigid erection phase, the cavernosus muscles'
infiltration with lidocaine effected a drop of the ICP to a mean of
69.5±7.6 cm H2O (range 60–77). Repeating the test
using normal saline instead of lidocaine did not affect the ICP.
The aforementioned results were reproducible with no significant difference (P > .05) when the test was repeated in the individual subject.
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Discussion |
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The mechanism of ICP elevation to the suprasystolic pressure level in the rigid erection phase is not fully elucidated. It could be due to excess blood entrapped in the cavernous tissue (Andersson and Wagner 1995). To what, however, can this extra blood entrapment be attributed? Our current study has revealed that the suprasystolic pressure during erection occurred in episodes associated with increased BCM and ICM EMG activity. This effect most likely confirms that the increased ICP is the result of cavernosus muscle contraction (Lavoisier et al 1988; Fournier et al, 1987; Andersson and Wagner 1995). The belt-form cavernosus muscles' insertion into the CC presumably constricts on contraction the dorsal penile vessels, with a resulting extra blood entrapment in the cavernous tissue. It was shown in this study that the increase of the cavernosus muscles' EMG was intermittent, which apparently denotes intermittent cavernosus muscle contraction. These intermittent muscle contractions seem to be due to the striated nature of the cavernosus muscles. Under normal physiologic conditions, striated muscles continue contraction for a period of 50–70 seconds, after which time they relax spontaneously (Guyton and Hall 1997). Muscle recontraction may occur after a few seconds.
The intermittent cavernosus muscle contraction during rigid erection seems to be advantageous. On cavernosus muscle contraction, the ICP increases to above the systolic pressure (Andersson and Wagner 1995) and the penile corpora are apparently transmitted into a high-tension closed cavity. Retention of this high-tension closed cavity for long periods during penile thrusting at coitus may lead to cavernosus tissue ischemia. Therefore, the intermissions in cavernosus muscle contractions allow for alterations in the periods of muscle contraction and relaxation during which the cavernous tissue could be well oxygenated, particularly because the periods of cavernosus muscle contraction are relatively short. These factors provide a natural mechanism that keeps the cavernous tissue well oxygenated and prevents its destruction by ischemia.
The Response of Cavernosus Muscles to Erection with Identification of the Corporo-Cavernosal Reflex
The cavernosus muscles' contraction on ICP increase postulates a reflex
relation between the 2 actions. The constancy of this relationship was assured
by reproducibility. Meanwhile, the reflex nature of this relationship is
evidenced by the absence of suprasystolic pressure response upon
anesthetization of the assumed 2 arms of the reflex arc, the cavernous tissue
and the cavernosus muscles. We call this reflex relationship the
"corporocavernosal reflex" (CCR). It seems that ICP increase to a
certain level stimulates the intracavernosal pressure receptors to send
impulses to the spinal cord. These impulses are probably transmitted via the
pudendal nerve to the cavernosus muscles, effecting their contraction with a
resulting increase of the cavernosal pressure. It may be necessary to note
that lidocaine does not block the muscle activity but rather the sensory
fibers (C and A 
-fibers) which are responsible for pain and reflex
activity (Yokoyami et al,
2000; Silva et al,
2002).
It appears that the ICP increase to the systolic pressure during erection constitutes the stimulus for activation of the intracavernosal pressure receptors and evoking of the CCR. When, during erection, the ICP reaches a certain level, the CCR is evoked with resulting cavernosus muscle contraction, suprasystolic cavernosal pressure elevation, and rigid erection. Apparently, this rigid erection improves the quality of the sexual act for both partners, as it allows for penile thrusting deep into the vagina, thus augmenting sexual arousal.
In conclusion, cavernosal muscle contraction on corporal pressure elevation seems to be reflex and mediated through the CCR. Cavernosal muscle contraction effects ICP increase, which apparently leads to rigid erection. Changes in the evoked response amplitude would indicate a defect in the reflex pathway. The CCR might thus act as a diagnostic tool in the investigation of erectile dysfunction; this, however, needs further studies.
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Acknowledgments |
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Footnotes |
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References |
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Breza J, Aboseif SR, Orvis BR, Lue TF, Tanagho EAl. Detailed anatomy of penile neurovascular structures: surgical significance. J Urol. 1989;141: 437 –443.[Medline]
Fournier GR, Juenemann KP, Lue TF, Tanagho EA. Mechanisms of venous occlusion during canine penile erection: an anatomic demonstration. J Urol. 1987;137: 163 –167.[Medline]
Goldstein AM, Padma-Natham H. The microarchitecture of the intracavernosal smooth muscle and the cavernosal fibrous skeleton. J Urol. 1990;144: 1144 –1146.[Medline]
Guyton AC, Hall JE. Contraction of skeletal muscle. In: Guyton AC, Hall JE, eds. Human Physiology and Mechanisms of Disease. 6th ed. Philadelphia, Pa: WB Saunders Co; 1997; 59–70.
Lavoisier P, Proulx J, Courtois F, de Carufel F, Durandl LG. Relationship between perineal muscles contractions, penile tumescence and penile rigidity during nocturnal erections. J Urol. 1988; 139: 176 –179.[Medline]
Lue TF, Broderick G. Evaluation and non-surgical management of erectile dysfunction and priapism. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Campbell's Urology. 7th ed. Philadelphia, Pa: WB Saunders Co; 1998: 1181 –1214.
Lue TF, Tanagho EA. Hemodynamics of erection. In: Tanagho EA, Lue TF, McClure RD, eds. Contemporary Management of Impotence and Infertility. 1st ed. Baltimore, Md: Williams & Wilkins; 1988 : 28–38.
Saenz de Tejada I, Moronkian P, Tessier J, Kim JJ, Goldstein I, Frohrib D. Trabecular smooth muscle modulates the capacitor function of the penis: studies on a rabbit model. Am J Physiol. 1991; 261: H1078 –H1085.
Silva C, Ribeiro MI, Cruz F. The effect of intravesical resiniferatox in patients with idiopathic detrusor instability suggests that involuntary detrusor contractions are triggered by C-fiber input. J Urol. 2002;168: 575 –579.[CrossRef][Medline]
Skandalakis JE, Colborn GL, Weidman TA, Badalament RA, Scaljon WM, Parrott TS, Galloway NTM, Mirrilas P. Male genital system. In: Skandalakis JE, ed. Skandalakis' Surgical Anatomy: The Embryologic and Anatomic Basis of Modern Surgery. 1st ed. Athens, Greece: Paschalidis Medical Publications; 2004: 1381 –1473.
Yokoyami O, Komatso K, Kodama K, Yotsuyanagi S, Nukura S, Namiki M. Diagnostic value of intravesical lidocaine for overactive bladder. J Urol. 2000;164: 340 –343.[CrossRef][Medline]
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= intracorporal pressure of 150 cm H2O.