ABSTRACT
PURPOSE: Although many clinical observations support the idea that denervation may cause erectile dysfunction, there has been suggested as an underlying cause, resulting in decreased penile tissue and consequently impotence. This study was initiated to investigate whether apoptosis follows denervation of the rat penis. MATERIALS AND METHODS: A total of 40 male Sprague-Dawley rats (10 weeks old) underwent abdominal exploration and unilateral or bilateral cavernous neurotomy. The penises were collected following sacrifice of animals at postoperation day 1, 2, 3, 6, or 10. Sham-operated animals served as controls. Tissues were embedded in paraffin and 3-?3 sections obtained. Deoxyribonucleic acid (DNA) fragmentation was analyzed by an in situ end-labeling method and by gel electrophoresis. Immunohistochemical study was carried out using monoclonal antibodies to p53. RESULTS: DNA fragmentation was evident in the tissues. In situ labeling revealed that the number of apoptotic bodies increased in tandem with the length of denervation. This finding was confirmed by electrophoretic analysis of DNA. However, there was no difference between the unilaterally and bilaterally treated groups. Immunohistochemical localization showed that p53 expression was increased in tissue sections of denervated animals, whereas little or no expression was shown in normal controls. CONCLUSIONS: Our results demonstrate that denervation causes apoptotic cell death in the rat penis. It is also suggested that unilateral nerve injury may be sufficient to affect normal erectile function. Further study will elucidate the molecular mechanisms of impotence caused by nerve-damaging operations such as prostatectomy.
Subject(s)
Animals , Humans , Male , Rats , Antibodies, Monoclonal , Apoptosis , Cell Death , Denervation , DNA , DNA Fragmentation , Electrophoresis , Erectile Dysfunction , Muscle, Smooth , Myocytes, Smooth Muscle , Paraffin , Penis , Prostatectomy , Rats, Sprague-DawleyABSTRACT
PURPOSE: We performed this study to determine the value of pharmacoerection with PGE1 for measurement of conduction velocity in the dorsal penile nerve and to identify the change in sensation in the glans penis between th pre-erection and posterection state. MATERIALS AND METHODS: We studied 14 patients with psychogenic impotence and premature ejaculation (mean age 45.2+/-6.5 years) who had no evidence of neurologic deficit and responded with a full erection lasting more than 1 hour to PGE1 injection. We measured penile length, penile temperature, sensory threshold of the glans penis to electrical stimulation, BCRL, pudendal sensory evoked potential (SEP), and dorsal nerve conduction velocity and amplitude before, directly after, and 1 hour after erection induced using PGE1(15~20 microgram). RESULTS: Neither PGE1 nor prolonged erection had any effect on the sensory threshold of glans penis, BCRL, pudendal SEP, or amplitude of the dorsal verve. Only the dorsal nerve conduction velocity changed. We could check the conduction velocity after erection in therr cases in which these values were not available at rest. CONCLUSIONS: Given the absence of change in the sensory condition of the glans penis, pharmacoerection using PGE1 has no effect on premature ejaculation except to prolong the erection state. Pharmacoerection seems to be the best method of calculating dorsal nerve sensory conduction velocity and amplitude, It can replace th normal erection state and also help in obtaining a recordable potential when this measurement is technically difficult at rest.
Subject(s)
Humans , Male , Alprostadil , Electric Stimulation , Erectile Dysfunction , Evoked Potentials , Neural Conduction , Neurologic Manifestations , Penis , Premature Ejaculation , Pudendal Nerve , Sensation , Sensory ThresholdsABSTRACT
PURPOSE: Although many clinical observations support the idea that denervation may cause erectile dysfunction, there has been suggested as an underlying cause, resulting in decreased penile tissue and consequently impotence. This study was initiated to investigate whether apoptosis follows denervation of the rat penis. MATERIALS AND METHODS: A total of 40 male Sprague-Dawley rats (10 weeks old) underwent abdominal exploration and unilateral or bilateral cavernous neurotomy. The penises were collected following sacrifice of animals at postoperation day 1, 2, 3, 6, or 10. Sham-operated animals served as controls. Tissues were embedded in paraffin and 3-?3 sections obtained. Deoxyribonucleic acid (DNA) fragmentation was analyzed by an in situ end-labeling method and by gel electrophoresis. Immunohistochemical study was carried out using monoclonal antibodies to p53. RESULTS: DNA fragmentation was evident in the tissues. In situ labeling revealed that the number of apoptotic bodies increased in tandem with the length of denervation. This finding was confirmed by electrophoretic analysis of DNA. However, there was no difference between the unilaterally and bilaterally treated groups. Immunohistochemical localization showed that p53 expression was increased in tissue sections of denervated animals, whereas little or no expression was shown in normal controls. CONCLUSIONS: Our results demonstrate that denervation causes apoptotic cell death in the rat penis. It is also suggested that unilateral nerve injury may be sufficient to affect normal erectile function. Further study will elucidate the molecular mechanisms of impotence caused by nerve-damaging operations such as prostatectomy.
Subject(s)
Animals , Humans , Male , Rats , Antibodies, Monoclonal , Apoptosis , Cell Death , Denervation , DNA , DNA Fragmentation , Electrophoresis , Erectile Dysfunction , Muscle, Smooth , Myocytes, Smooth Muscle , Paraffin , Penis , Prostatectomy , Rats, Sprague-DawleyABSTRACT
PURPOSE: We performed this study to determine the value of pharmacoerection with PGE1 for measurement of conduction velocity in the dorsal penile nerve and to identify the change in sensation in the glans penis between th pre-erection and posterection state. MATERIALS AND METHODS: We studied 14 patients with psychogenic impotence and premature ejaculation (mean age 45.2+/-6.5 years) who had no evidence of neurologic deficit and responded with a full erection lasting more than 1 hour to PGE1 injection. We measured penile length, penile temperature, sensory threshold of the glans penis to electrical stimulation, BCRL, pudendal sensory evoked potential (SEP), and dorsal nerve conduction velocity and amplitude before, directly after, and 1 hour after erection induced using PGE1(15~20 microgram). RESULTS: Neither PGE1 nor prolonged erection had any effect on the sensory threshold of glans penis, BCRL, pudendal SEP, or amplitude of the dorsal verve. Only the dorsal nerve conduction velocity changed. We could check the conduction velocity after erection in therr cases in which these values were not available at rest. CONCLUSIONS: Given the absence of change in the sensory condition of the glans penis, pharmacoerection using PGE1 has no effect on premature ejaculation except to prolong the erection state. Pharmacoerection seems to be the best method of calculating dorsal nerve sensory conduction velocity and amplitude, It can replace th normal erection state and also help in obtaining a recordable potential when this measurement is technically difficult at rest.