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Seminal emission from the ejaculatory duct (SEED) by direct electrical stimulation of the vas deferens was investigated in the dog, and the technique was applied to men. The stimulus parameters used were 2 msec, 10 Hz, and 8 V for dogs or 15–20 V for humans. In vitro studies using tetrodotoxin demonstrated that the major portion of the muscle contraction under the above stimulation was neurogenic. The stimulation of the pars epididymica, the middle vas, or the ampulla of the vas caused SEED in all dogs having intact hypogastric nerves (HNs) and receiving transection of bilateral HNs 1, 6, and 12 months before electrical stimulation. The dye instilled into the canine cauda epididymis was transported to the ampulla and emitted into the posterior urethra by electrical stimulation of the vas regardless of the site stimulated. The electrical stimulation of eight vasa deferentia (pars epididymica) of five prostatic carcinoma patients generated emission from the severed proximal end of all vasa examined at orchidectomy. All of the stimulations of 13 middle vasa of seven patients with emission loss caused SEED. The above results indicate that direct electrical stimulation of the canine and human vas deferens causes SEED regardless of the site stimulated or the absence of HNs, which are the major pathway of the efferent signal for SEED.
Seminal emission from the ejaculatory duct (SEED) by direct electrical stimulation of the vas deferens was investigated in the dog, and the technique was applied to men. The stimulus parameters used were 2 msec, 10 Hz, and 8 V for dogs or 15–20 V for humans. In vitro studies using tetrodotoxin demonstrated that the major portion of the muscle contraction under the above stimulation was neurogenic. The stimulation of the pars epididymica, the middle vas, or the ampulla of the vas caused SEED in all dogs having intact hypogastric nerves (HNs) and receiving transection of bilateral HNs 1, 6, and 12 months before electrical stimulation. The dye instilled into the canine cauda epididymis was transported to the ampulla and emitted into the posterior urethra by electrical stimulation of the vas regardless of the site stimulated. The electrical stimulation of eight vasa deferentia (pars epididymica) of five prostatic carcinoma patients generated emission from the severed proximal end of all vasa examined at orchidectomy. All of the stimulations of 13 middle vasa of seven patients with emission loss caused SEED. The above results indicate that direct electrical stimulation of the canine and human vas deferens causes SEED regardless of the site stimulated or the absence of HNs, which are the major pathway of the efferent signal for SEED.
Sympathetic denervation of the rat cauda epididymidis by surgical removal of the inferior mesenteric ganglion (IMG) results in an excessive accumulation of sperm in the cauda epididymidis as well as significant changes in cauda sperm motility and cauda epididymal gross histology. The objective of the present study was to determine if the cauda‐specific changes in sperm storage, sperm motility, and epididymal histology following the loss of sympathetic innervation were accompanied by changes in the protein composition of epididymal fluid. One and 4 weeks after surgical IMG removal or sham operations, luminal fluid obtained from the caput and cauda epididymidis and cauda epididymal sperm‐associated proteins were subjected to two‐dimensional polyacrylamide gel electrophoresis (2‐D PAGE) and silver‐stained proteins were quantitated. One week after IMG removal, two cauda epididymal fluid (CEF) proteins (2 and 13) had increased 43% and 49%, respectively, whereas four CEF proteins (5, 8, 9, and 19) had decreased between 30% and 73% compared to controls. Four weeks after IMG removal, changes in CEF proteins observed 1 week following surgery were no longer present, but the staining intensities of three additional CEF proteins (11, 12, and 18) were reduced an average of 70% compared to control CEF proteins. By obstructing the cauda epididymidis, we confirmed that the changes in CEF protein composition observed following IMG removal were not the result of sperm accumulation but were due directly to the loss of innervation; the staining intensity of CEF protein 2 increased as a result of excessive sperm accumulation in the cauda epididymidis both in the presence and absence of innervation from the IMG. No significant changes in caput epididymal fluid proteins or cauda epididymal sperm‐associated proteins were detected following IMG removal. These data show that the protein composition of rat CEF is significantly affected by the loss of sympathetic innervation and suggest that neuronal input may play an important role in the maintenance of epididymal function.
The rat cauda epididymidis receives sympathetic innervation from the inferior mesenteric ganglion (IMG). We have previously demonstrated that surgical removal of the IMG and proximal hypogastric nerves (IMG denervation) results in significant and cauda‐specific changes in epididymal sperm transport, sperm motility, luminal fluid protein composition, and tissue histology. In the present study we used natural mating trials and intrauterine insemination (IUI) techniques to determine whether or not IMG denervation affects male fertility and reproductive capacity. For the initial studies, adult male Sprague Dawley rats were mated with estrous females 1 and 4 weeks following IMG denervation. Nine days after mating, uterine implantation sites and corpora lutea (CL) were counted. In females mated with sham‐operated control males, 85.8% of ovulated oocytes were fertilized and subsequently implanted. In contrast, females mated with IMG‐denervated males 1 or 4 weeks following surgery had 0% and 3.5%, respectively, of ovulated oocytes fertilized and implanted. For rats maintained 21 days after mating, an average of 13 ± 1 pups were delivered by each of nine females mated with sham‐operated control male rats; whereas, only seven morphologically normal pups were delivered by one of 14 females mated with IMG‐denervated male rats. Additional experiments demonstrated that the decrement in offspring was, in part, due to a significant decrease in the number of spermatozoa in the female uterus following mating with IMG‐denervated males. To determine whether IMG denervation exerted an additional effect directly on the fertilizing ability of spermatozoa, IUI experiments were performed. Six million cauda epididymal spermatozoa from 1‐ or 4‐week IMG‐denervated males were inseminated into the uterine horns of luteinizing hormone‐releasing hormone (LHRH)‐synchronized females and 9 days later implantation sites and CL were counted. Implantations were observed for 78%, 28%, and 25% of ovulated oocytes following IUI with spermatozoa from sham‐operated controls and from 1 ‐ and 4‐week IMG‐denervated rats, respectively. To determine whether the reduction in implantation sites following IUI with spermatozoa from IMG‐denervated rats resulted from impaired oocyte fertilization, studies were performed in which oocytes were retrieved and stained 24 hours after IUI. Comparable fertilization rates of 76.5% and 89.0% were observed using cauda epididymal spermatozoa from IMG‐denervated and sham‐operated control males, respectively, indicating that oocyte fertilization was not affected by the loss of innervation. These studies establish the importance of innervation from the IMG for ejaculatory competence and sperm reproductive capacity in the male rat. These data further suggest that sympathetic innervation in the epididymis critically influences paternal factors associated with embryonic development.
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