Irvin E. Lawrence

The Effect of Denervation on Compensatory Ovarian Hypertrophy

Hemiovariectomized rats were randomly assigned to 1 of 5 groups: controls, 6-hydroxydopamine (6-HD)-treated, abdominal vagotomy, 6-HD-treated plus abdominal vagotomy and pelvic parasympathectomy. 15 days later all animals were sacrificed and the amount of compensatory ovarian hypertrophy (COH) was calculated. Vagotomy and vagotomy plus 6-HD treatment interrupted estrous cycles and significantly decreased COH. Vagotomized rats with both ovaries intact had disrupted estrous cycles but ovarian weights were not affected. In a subsequent study, rats in estrus were sham-operated, unilaterally ovariectomized (ULO), vagotomized, or vagotomized + ULO, and serum levels of LH and FSH were determined at 5 and 24 h. ULO caused a significant (p less than 0.05) increase in LH and FSH at 5 h. Vagotomy significantly (p less than 0.05) depressed LH and FSH levels in hemiovariectomized animals at 5 h. By 24 h LH was significantly higher in ULO than in either sham-operated (p less than 0.05) or vagotomy (p less than 0.01) groups. Also, vagotomy significantly (p less than 0.01) depressed FSH levels at 24 h. These results suggest a functional role for the vagus nerve in normal cyclic activity, COH, and gonadotrophin (Gn) secretion.

Effects of Abdominal Vagotomy on the Estrous Cycle of the Rat and the Induction of Pseudopregnancy

Abdominal vagotomy of estrus or proestrus rats resulted in disruptions of the estrous cycle which was characterized by prolonged periods of diestrus (10-12 days in length). In contrast, vagotomy on metestrus or diestrus did not disrupt the estrous cycle. The induction of pseudopregnancy, in response to cervical stimulation on the morning of estrus, was also interrupted by abdominal vagotomy. The nocturnal and diurnal prolactin surges and elevations in serum progesterone, characteristic of pseudopregnancy, were prevented by vagotomy. Vagotomy, also, largely prevented the formation of deciduoma in response to traumatization of the uterus in cervically stimulated rats.

The adrenergic innervation of the guinea pig ovary during prenatal and postnatal periods

The pattern of adrenergic nerves was visualized and norepinephrine (NE) quantified in guinea pig ovaries from fetal day 50 to term and on days 1, 5, 10, 20 and 28 postnatally. Before birth, there were a few perivascular adrenergic nerves and correspondingly low ovarian NE levels. After birth and through day 20, nerves gradually grew into adjacent stroma. By day 28, there was a proliferation of beaded adrenergic nerves around blood vessels and into adjacent stroma, which was reflected by significantly increased ovarian levels of NE. These findings are discussed in relation to antral follicle development, atresia, and interstitial gland formation in the ovaries of prepubertal guinea pigs.

Prostaglandin F2alpha prostaglandin E2, progesterone, 20alpha-dihydroprogesterone and ovarian 20alpha hydroxysteroid dehydrogenase activity in preparturient pelvic neurectomized rats.

Summary Several workers have reported that section of the pelvic parasympathetic nerves [pelvic neurectomy (PN)] in pregnant rats is compatible with pregnancy, but parturition is blocked. The cause of this blocked parturition remains unexplained. To determine if PN had a possible action on progesterone and prostaglandin, two endocrine mediators of labor, we neurectomized (PN) or sham-operated (S) rats on days 8-10 of pregnancy. Then on days 20, 21, 22, 23 and 24 (PN only) rats were lightly etherized and utero-ovarian vein (UOV) blood was collected, centrifuged and plasma frozen and stored at −60° until radioimmunoassay for progesterone, 20α-dihydroprogesterone (20α-ol), prostaglandin F2α (PGF), and prostaglandin E2 (PGE). One ovary from each rat was immersed in a BEEM capsule containing OCT compound, frozen and stored at −20° for 20α-hydroxysteroid dehydrogenase (20α-HSD) histochemistry. Analysis of variance indicated a significant (P < 0.01) decline in plasma progesterone in the S animals on the days studied but the PN animals remained unchanged through day 22. Students Newman-Keuls (SNK) analysis for multiple critical values indicated that plasma progesterone on days 20 and 21 was not different in the S animals but declined (P < 0.01) on day 22. Progesterone also declined on days 23 and 24 in PN animals. There was a significant increase (P < 0.05) between day 20, 21 and 22 plasma PGF in the S but no change in the plasma PGF in the PN animals on any of these days or on days 23 and 24. SNK analysis showed increased PGF (P < 0.05) on day 22 in the S animals. But UOV PGE did not change in the PN or S groups. The density and intensity of ovarian 20α-HSD reaction product was low in both S and PN rats on days 20 and 21. Increased density and intensity of ovarian 20α-HSD reaction product was characteristic of five animals on day 22 and PN rats on days 22, 23 and 24. Collectively, these results indicate that the pelvic nerves participate in the orchestration of endocrine and uterine events in the pre-parturient and parturient periods in the rat.

Effect of Abdominal Vagotomy at Proestrus on Ovarian Weight, Ovarian Antral Follicles, and Serum Levels of Gonadotropins, Estradiol, and Testosterone in the Rat

The effects of abdominal vagotomy at proestrus on ovarian weight and antral follicles greater than 150 microns diameter and on serum levels of gonadotropins and testosterone were assessed 24 and 48 h and 4 and 8 days after surgery. Serum levels of estradiol were assessed at 4 and 8 days. Vagotomy increased ovarian weight at 48 h, decreased ovarian weight at 4 days, but had no effect by day 8. Vagotomy increased healthy antral follicles 151-394 microns diameter at 24 and 48 h and increased atresia in this size range at 4 and 8 days. Vagotomy decreased healthy follicles 151-384 microns at day 8. Vagotomy decreased healthy follicles 395-570 microns at 24 h and decreased atretic follicles at 48 h. Vagotomy decreased the largest (over 570 micron diameter) healthy follicles at 24 h and 8 days. Vagotomy decreased basal serum LH levels at 48 h and 8 days. (In contrast, vagotomy increased FSH at 24 h). There was no effect on blood levels of estradiol and testosterone. These findings are discussed in relation to the hypothesis that the vagus nerve is a component of the hypothalamo-hypophyseal-ovarian axis.

Effect of Vagotomy on Postcastration Gonadotropin Secretion in Male Rats

Abstract The postcastration increase in gonadotropins was studied in intact and vagotomized male rats. Rats underwent vagotomy or sham surgery immediately prior to castration. In the first experiment, rats were bled before castration and at 1,2, 4, and 7 days after castration. Serum LH and FSH were significantly lower in vagotomized rats 1 day after castration. On Days 2, 4, and 7 postcastration, serum gonadotropin levels were generally not different among experimental groups. In a second experiment, rats were decapitated at 12 or 24 hr after surgery and castration. Trunk blood was collected for assay of LH. Vagotomy had no effect on LH levels at 12 hr postcastration, but, at 24 hr postcastration, vagotomized rats had significantly lower serum LH than did sham-operated rats. These experiments indicate that vagotomy has a transient suppressive effect on gonadotropin release following castration. Such observations support the hypothesis that the vagus nerve may play a modulatory role in gonadotropin secretion.

Abdominal Vagotomy Does Not Activate the Corpus luteum in Rats

Rats were vagotomized at proestrus and 4 days later serum prolactin and progesterone were determined by radioimmunoassay. The histology of the ovaries and the activity of ovarian delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) were also studied. There was no difference between hormone values in sham and vagotomized rats 4 days after surgery. In addition, the ovarian histology and activity of 3 beta-HSD were similar in both sham and vagotomized animals. We conclude that vagotomy at proestrus does not interrupt estrous cycles by activating the corpus luteum.

Depletion of tuberoinfundibular dopamine does not restore gonadotropin secretion in ovariectomized hyperprolactinemic rats

The effect of depleting tuberoinfundibular dopamine (TIDA) on gonadotropin secretion was studied in rats made hyperprolactinemic by implantation of the prolactin and growth hormone secreting Furth MtTW15 tumor. Implants of the pituitary tumor prevented gonadotropin release in response to castration. Daily injection of 100 mg dl-alpha-methyl-para-tyrosine/kg bw which reduced TIDA levels in tumor bearing rats more than 90% did not restore gonadotropin release. It seems likely that the increased activity of the TIDA system does not mediate the suppression of gonadotropins during chronic hyperprolactinemia.

Inhibition of Hypothalamic LHRH Depletion after Ovariectomy by Transplantable Prolactin and Growth-Hormone-Secreting Tumors

Abstract Anestrous Wistar-Furth rats bearing implants of the Furth MtTW15 tumor and diestrous tumor-free rats were ovariectomized and serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) concentrations, and hypothalamic luteinizing hormone-releasing hormone (LHRH) content, were studied. The increase of LH and FSH, after ovariectomy, was significantly greater in tumor-free rats than in rats bearing prolactin secreting tumor implants. The hypothalamic LHRH content of the intact tumor-bearing rats was greater (P < 0.01) than that of tumor-free rats. Furthermore, the depletion of hypothalamic LHRH content was greater in tumor-free rats than in tumor-bearing rats. These results suggest that this prolactin and growth-hormone-secreting tumor prevents gonadotropin release by reducing LHRH release from the hypothalamus.