On the pathogenesis of penile venous leakage: role of the tunica albuginea

<p>Abstract</p> <p>Background</p> <p>Etiology of venogenic erectile dysfunction is not exactly known. Various pathologic processes were accused but none proved entirely satisfactory. These include presence of large venous channels draining corpora cavernosa, Peyronie's disease, diabetes and structural alterations in fibroblastic components of trabeculae and cavernous smooth muscles. We investigated hypothesis that tunica albuginea atrophy with a resulting subluxation and redundancy effects venous leakage during erection.</p> <p>Methods</p> <p>18 patients (mean age 33.6 ± 2.8 SD years) with venogenic erectile dysfunction and 17 volunteers for control (mean age 31.7 ± 2.2 SD years) were studied. Intracorporal pressure was recorded in all subjects; tunica albuginea biopsies were taken from 18 patients and 9 controls and stained with hematoxylin and eosin and Masson's trichrome stains.</p> <p>Results</p> <p>In flaccid phase intracorporal pressure recorded a mean of 11.8 ± 0.8 cm H₂O for control subjects and for patients of 5.2 ± 0.6 cm, while during induced erection recorded 98.4 ± 6.2 and 5.9 ± 0.7 cmH₂O, respectively. Microscopically, tunica albuginea of controls consisted of circularly-oriented collagen impregnated with elastic fibers. Tunica albuginea of patients showed degenerative and atrophic changes of collagen fibers; elastic fibers were scarce or absent.</p> <p>Conclusion</p> <p>Study has shown that during erection intracorporal pressure of patients with venogenic erectile dysfunction was significantly lower than that of controls. Tunica albuginea collagen fibers exhibited degenerative and atrophic changes which presumably lead to tunica albuginea subluxation and floppiness. These tunica albuginea changes seem to explain cause of lowered intracorporal pressure which apparently results from loss of tunica albuginea veno-occlusive mechanism. Causes of tunica albuginea atrophic changes and subluxation need to be studied.</p

The hypoactive corpora cavernosa with degenerative erectile dysfunction: a new syndrome

BACKGROUND: In a group of 22 patients with erectile dysfunction, vasculogenic, neurogenic, endocrinologic or psychogenic investigations failed to find a cause for their erectile dysfunction. The electro-cavernosograms of these patients recorded a diminished activity. We investigated the hypothesis that diminished corpus cavernosum electromyography activity was the cause of erectile dysfunction in these patients. METHODS: The study comprised the above mentioned 22 patients (study group, 43.8 ± 5.9 SD years) and 15 healthy volunteers (control group, 41.8 ± 5.1 SD years). The electro-cavernosograms were recorded in the flaccid, erectile and detumescent phases by 2 electrodes inserted into the corpus cavernosum. RESULTS: The electro-cavernosogram of the healthy volunteers registered in the flaccid phase regular slow waves and random action potentials. The wave variables declined significantly in the erectile phase (p < 0.01). In the study group, the slow wave variables in the flaccid phase exhibited a significant decrease (p < 0.05) compared to the healthy volunteers, and the rhythm was irregular. Erection did not occur with sildenafil administration or intracavernosal papaverine injection, and penile implant was performed. Biopsy examination showed degenerated muscle fibers, and fragmented collagen and elastic fibers with areas of fibrosis. CONCLUSION: A novel concept of the cause of erectile dysfunction was presented. Corpora cavernosa showed degenerative changes on histopathologic examination and exhibited diminished electromyography activity. They did not respond to sildenafil administration or intracavernosal papaverine injection. Penile implants were the only treatment. The condition is given the name 'hypoactive corpus cavernosum'. The cause of corpus cavernosum degenerative changes needs further study

Electroesophagogram in gastroesophageal reflux disease with a new theory on the pathogenesis of its electric changes

BACKGROUND: In view of the disturbed esophageal peristaltic activity and abnormal esophageal motility in gastroesophageal reflux disease, (GERD), we investigated the hypothesis that these changes result from a disordered myoelectric activity of the esophagus. METHODS: The electric activity of the esophagus (electroesophagogram, EEG) was studied in 27 patients with GERD (16 men, 11 women, mean age 42.6 ± 5.2 years) and 10 healthy volunteers as controls (6 men, 4 women, mean age 41.4 ± 4.9 years). According to the Feussner scoring system, 7 patients had a mild (score 1), 10 a moderate (score 2) and 10 a severe (score 3) stage of the disease. One electrode was applied to the upper third and a second to the lower third of the esophagus, and the electric activity was recorded. The test was repeated after the upper electrode had been moved to the mid-esophagus. RESULTS: The EEG of the healthy volunteers showed slow waves and exhibited the same frequency, amplitude and conduction velocity from the 2 electrodes of the individual subject, regardless of their location in the upper, middle or lower esophagus. Action potentials occurred randomly. In GERD patients, score 1 exhibited electric waves' variables similar to those of the healthy volunteers. In score 2, the waves recorded irregular rhythm and lower variables than the controls. Score 3 showed a "silent" EEG without waves. CONCLUSION: The electric activity in GERD exhibited 3 different patterns depending on the stages of GERD. Score 1 exhibited a normal EEG which apparently denotes normal esophageal motility. Score 2 recorded irregular electric waves variables which are presumably indicative of decreased esophageal motility and reflux clearance. In score 3, a "silent" EEG was recorded with probably no acid clearance. It is postulated that the interstitial cells of Cajal which are the electric activity generators, are involved in the inflammatory process of GERD. Destruction of these cells appears to occur in grades that are in accordance with GERD scores. The EEG seems to have the potential to act as an investigative tool in the diagnosis of GERD stages

Effect of thermal cutaneous stimulation on the gastric motor activity: Study of the mechanism of action

AIM: To investigate the mechanism of action of thermal cutaneous stimulation on the gastric motor inhibition

Electromyographic activity of the anterolateral abdominal wall muscles during the vesical filling and evacuation

&lt;font face="TimesNewRoman,Bold" size="1"&gt;&lt;p align="left"&gt;&lt;strong&gt;BACKGROUND: &lt;/strong&gt;&lt;font face="TimesNewRoman" size="2"&gt;The role of the anterolateral abdominal wall muscles (AAWMs) during the vesical filling and evacuation has not been sufficiently addressed in the literature. We have investigated the hypothesis that the AAWMs exhibit the increased electromyographic (EMG) activity on the vesical distension and contraction which presumably assists vesical evacuation.&lt;/font&gt;&lt;/p&gt;&lt;/font&gt;&lt;font face="TimesNewRoman,Bold" size="1"&gt;&lt;p align="left"&gt;&lt;strong&gt;METHODS: &lt;/strong&gt;&lt;font face="TimesNewRoman" size="2"&gt;The effects of the vesical balloon distension on the vesical pressure (VP), vesical neck (VNP) pressures and the AAWMs&amp;#39; EMG activity were studied in 28 healthy volunteers aged 40.7 &amp;plusmn; 9.7 years (18 men, 10 women). These effects were tested after the individual anesthetization of the bladder and AAWMs and after saline infiltration.&lt;/font&gt;&lt;/p&gt;&lt;/font&gt;&lt;font face="TimesNewRoman,Bold" size="1"&gt;&lt;p align="left"&gt;&lt;strong&gt;RESULTS: &lt;/strong&gt;&lt;font face="TimesNewRoman" size="2"&gt;The VP and the VNP showed a gradual increase upon the incremental vesical balloon distension which started at a distending volume of 120&amp;ndash;140 ml. At a mean volume of 364.6 &amp;plusmn; 23.8 ml, the VP increased to a mean of 36.6 &amp;plusmn; 3.2 cmH&lt;/font&gt;&lt;font face="TimesNewRoman" size="1"&gt;2&lt;/font&gt;&lt;font face="TimesNewRoman" size="2"&gt;O, the VNP decreased to 18.4 &amp;plusmn; 2.4 cmH&lt;/font&gt;&lt;font face="TimesNewRoman" size="1"&gt;2&lt;/font&gt;&lt;font face="TimesNewRoman" size="2"&gt;O, and the AAWMs EMG registered a significant increase. This effect disappeared in the individual bladder and in the AAWMs&amp;#39; anesthetization. However, it did not disappear in the saline administration.&lt;/font&gt;&lt;/p&gt;&lt;/font&gt;&lt;font face="TimesNewRoman,Bold" size="1"&gt;&lt;p align="left"&gt;&lt;strong&gt;CONCLUSIONS: &lt;/strong&gt;&lt;font face="TimesNewRoman" size="2"&gt;The AAWMs appear to contract simultaneously with vesical contraction. This action presumably increases the IAP and it assists vesical contraction. The AAWMs contraction on vesical contraction seems to be mediated through a reflex which is called the &amp;#39;vesico-abdominal wall reflex&amp;#39;. Further studies are required to investigate the role of this reflex in vesical disorders.&lt;/font&gt;&lt;/p&gt;&lt;/font&gt;&lt;font face="TimesNewRoman,Bold" size="1"&gt;&lt;p align="left"&gt;&lt;strong&gt;KEY WORDS: &lt;/strong&gt;&lt;font face="TimesNewRoman" size="2"&gt;Oblique muscles, transversus abdominis, rectus abdominis, vesical pressure, electromyography.&lt;/font&gt;&lt;/p&gt;&lt;/font&gt