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PubMed1988

Influence of adrenalectomy on pancreatic enzyme secretion.

Both adrenalectomy and chemically induced diabetes mellitus cause a marked decrease of pancreatic amylase synthesis in rats. Diabetes is further associated with alterations of cholecystokinin (CCK)-stimulated enzyme secretion. Using isolated pancreatic acini prepared from adrenalectomized male rats, we investigated the effects of adrenalectomy on pancreatic enzyme secretion. CCK8-stimulated amylase secretion showed a typical biphasic dose-response curve in acini from both adrenalectomized and sham-operated animals with similar basal secretions, similar sensitivities to various CCK8 concentrations, but a statistically significant elevation of maximal amylase secretion after adrenalectomy. Receptor-binding studies with 125I-BH-CCK8 revealed an increase of binding to the high-affinity part of the CCK receptor in adrenalectomized rats. While carbachol-stimulated secretion showed no changes in maximal secretion rates, it did show a decrease in sensitivity in adrenalectomized animals with a statistically significant shift to the right of the dose-response curves. Competitive inhibition curves with 3H-N-methylscopolamine and carbachol as the competitive receptor agonist showed no differences in receptor binding between controls and adrenalectomized rats. We propose that complex alterations in hormone/neurotransmitter-stimulated pancreatic enzyme secretion are found in glucocorticoid depletion, explainable via a postreceptor defect in carbachol-stimulated secretion. The functional and binding data with regard to CCK are more difficult to explain.

Adrenal Glands↗
PubMed1983

Developmental changes in fetal adrenal hypertrophy following maternal bilateral and fetal unilateral adrenalectomy at different stages of gestation in the rat.

Maternal adrenalectomy on days 14 and 15 of gestation did not alter the fetal adrenal weight 2 days later. The same operation on day 16 caused a significant increase in the adrenal weight with a hypertrophy of the cortical cells. Nevertheless, the operation on days 17 and 18 induced no change in the fetal adrenals. Subsequently on days 19 and 20, the operation resulted in a significant hypertrophy of the fetal adrenals. Fetal unilateral adrenalectomy on day 18 caused, 2 days later, significant hypertrophy of the contralateral adrenal, in contrast with no significant change after maternal adrenalectomy. This is perhaps due to the difference in the amount of fetal plasma corticoids, as evidenced by the previous reports of high concentrations of fetal plasma corticosterone on days 19 and 20. The overall results suggest that the fetal pituitary-adrenal feedback mechanism begins to appear between days 16 and 18 of gestation.

Adrenal Glands↗
PubMed1987

Adrenalectomy and pentagastrin effects on gastrointestinal cholinergic enzyme activities.

The present study examined the effects of pentagastrin and adrenalectomy on choline acetyltransferase (ChAT) and acetylcholine esterase (AChE), enzymes which synthesize and degrade acetylcholine in the rat gastrointestinal tract. Adrenalectomized and non-adrenalectomized rats, 14 and 21 days old, were treated with either pentagastrin (250 micrograms/kg i.p.) or saline for 7 days. Rats were sacrificed at 21 and 28 days of age. Adrenalectomy- and pentagastrin-treated 21-day-old rats had greater ChAT activities than those treated with pentagastrin alone, while AChE activities were higher in the pentagastrin-treated group. Adrenalectomy- and pentagastrin-treated 28-day-old rats had lower levels of activity as compared to pentagastrin-treated rats. The adrenal gland does appear to influence the response of cholinergic enzyme activities to pentagastrin.

Acetylcholinesterase↗
PubMed1996

Technique and results of laparoscopic adrenalectomy.

OBJECTIVES: Our technique of laparoscopic adrenalectomy as well as the results of this method are presented. METHODS: Transperitoneal laparoscopic adrenalectomy was performed in 18 consecutive patients (10 right side, 8 left side) for Conn's disease (7 patients), pheochromocytoma (6 patients), Cushing's syndrome (1 patient), and large inactive adenoma (4 patients). The tumor size ranged between 1 and 8 cm (mean 4.2). One of the patients, who presented with Conn's disease and bilateral adenoma, underwent enucleation of the larger adenoma on the right side leaving the uninvolved portion of the adrenal gland intact. RESULTS: The mean operative time was below 3 h; blood loss was minimal in all cases except 2. Hypertensive crisis was not encountered in this series. The only postoperative complication seen was transient diabetes insipidus which occurred in 1 patient. Analgesics were required only on the first 2 postoperative days. Oral intake and ambulation were resumed within 24 h. Mean postoperative hospitalization was 4.6 days. CONCLUSIONS: In our hands, laparoscopic adrenalectomy proved to be associated with a low morbidity and few complications. In addition, it is one of the few procedures where laparoscopy can compete with open surgery in terms of operative time.

Adrenal Gland Neoplasms↗
PubMed1982

Adrenalectomy decreases the sphingomyelin and cholesterol content of fat cell ghosts.

Adrenalectomy produces a significant fall in the sphingomyelin and cholesterol content of ghosts isolated from rat epididymal fat cells. Previous studies from this laboratory have demonstrated an effect of dexamethasone in vitro to increase the sphingomyelin content of fat cell ghosts obtained from adrenalectomized animals. The present study demonstrates that adrenalectomy influences the membrane lipid content. Dexamethasone, in vitro, was found to increase the sphingomyelin of epididymal fat cell ghosts isolated from intact animals, as it previously had been shown to affect epididymal fat cell ghosts obtained from adrenalectomized animals. Incubation with dexamethasone for 3 h had no effect on the cholesterol content of the ghosts. Adrenalectomy, on the other hand, resulted in a significant decrease in the cholesterol content of the fat cell ghosts.

Adipose Tissue↗
PubMed1985

Regulation of corticotropin-releasing factor (CRF) receptors in the rat pituitary gland: effects of adrenalectomy on CRF receptors and corticotroph responses.

The stimulation of ACTH release from anterior pituitary cells by corticotropin-releasing factor (CRF) is mediated by specific, high affinity receptors with a Ka of 10(9) M-1 for ovine CRF. The relationship between ACTH secretion and CRF receptor activation was analyzed in normal and adrenalectomized rats by comparison of ACTH release with changes in CRF receptors and adenylate cyclase activity. The marked increase in plasma ACTH levels that occurred after adrenalectomy (from 71 to 478 pg/ml after 4 days) was accompanied by a progressive decrease in pituitary CRF receptor concentration [by 29 +/- 1%, 75 +/- 2%, 77 +/- 6%, and 80 +/- 4% (+/- SE) after 1, 2, 3, and 4 days, respectively]. Most of this decrease was due to receptor down-regulation rather than occupancy by endogenous CRF, since high dose infusions of CRF (300-500 ng/min) for 30 min before pituitary membrane preparation reduced CRF-binding sites by only 40%. The marked reduction in CRF receptors after adrenalectomy was accompanied by comparable decreases in maximal CRF-stimulated adenylate cyclase activity and sensitivity to CRF (ED50, 3.8 +/- 2.8 vs. 58 +/- 3.7 X 10-9 M CRF in control and 2-day-adrenalectomized rats, respectively). Fluoride-stimulated adenylate cyclase activity was unchanged at 24 h, but was decreased by 28 +/- 7% at later times. Such decreases in CRF receptors and adenylate cyclase activity in adrenalectomized rats were prevented by dexamethasone treatment. In cultured anterior pituitary cells from 4-day-adrenalectomized rats, CRF-stimulated cAMP production was decreased by 40%. However, in contrast to the decreases in CRF receptors and cAMP production, there was a 3-fold increase in CRF-stimulated ACTH release, with no change in sensitivity to CRF. The ability of corticotrophs to maintain increased ACTH release, in conjunction with reduced CRF receptors and CRF-stimulated adenylate cyclase, indicates that elevated ACTH secretion can be maintained by occupancy and activation of only a small number of CRF receptors. This finding also suggests that synergistic interactions between CRF and other regulators of ACTH release may contribute to the sustained increase in ACTH secretion that follows adrenalectomy.

Adenylyl Cyclases↗
PubMed1990

Induction of fos-like immunoreactivity in hypothalamic corticotropin-releasing factor neurons after adrenalectomy in the rat.

To identify brain sites responding to the removal of corticosterone feedback by adrenalectomy (ADX), rat brains were processed for fos immunocytochemistry 1, 3, and 7 days after ADX, sham-ADX, or no surgery using a polyclonal antiserum to fos residues 132-154. Compared to SHAM, ADX rats exhibited strong fos-like immunoreactivity (FLI) only in the parvocellular neurons of the paraventricular hypothalamic nuclei (PVN) 1, 3, and 7 days after surgery. Replacement with a corticosterone pellet at the time of adrenalectomy (ADX + B) prevented this increase in PVN FLI in three of four rats at 1 day, all rats at 3 days, and two of seven rats 7 days after surgery; 100 micrograms/ml corticosterone in the drinking water for 2 days before perfusion reversed ADX-induced increases in PVN FLI in 7-day ADX rats. Providing 25 micrograms/ml corticosterone in the drinking water to ADX rats for 5 days after surgery did not prevent expression of PVN FLI, even though this dose has been shown to normalize morning basal ACTH levels in ADX rats. Virtually all parvocellular PVN neurons expressing FLI after ADX costained for CRF. Some parvocellular neurons also expressed both fos and vasopressin. In all rats, many brain regions expressed FLI that was not related to adrenalectomy. We conclude that the changes in neuronal FLI correlate with demonstrated changes in neuroendocrine activity after ADX; however, suppression of ADX-induced FLI may require higher replacement levels of corticosterone than inhibition of ADX-induced ACTH secretion.

Adrenalectomy↗
PubMed1991

Effect of adrenalectomy or long term cortisol or adrenocorticotropin (ACTH)-releasing factor infusion on the concentration and molecular weight distribution of ACTH in fetal sheep plasma.

It is unclear whether the maturation of corticotrophs from the fetal to the adult type in the fetal sheep pituitary in late gestation is associated with changes in the sensitivity of the fetal pituitary to corticotrophic secretagogues and in the form of ACTH-containing peptides (IR-ACTH) secreted into the circulation. The maturation of the pituitary corticotroph population is known to be accelerated by intrafetal cortisol infusion and delayed by bilateral fetal adrenalectomy. We have therefore investigated the mol wt profile of IR-ACTH present in fetal sheep plasma from 110 days gestation until term (147 +/- 3 days) and determined whether intrafetal cortisol infusion between 105-117 days (2.5 mg cortisol/day), or bilateral fetal adrenalectomy can alter the mol wt profile of IR-ACTH in fetal sheep plasma. We have also investigated whether prior exposure to cortisol alters the subsequent responsiveness of the fetal pituitary to a long term infusion of ovine (o) CRF (10 micrograms oCRF/day). In the control group, the proportion of IR-ACTH which eluted in the low-mol wt (LMW) range (i.e. less than 12K) was significantly higher between 121-125 days (43.9 +/- 4.2%) than between 126-139 days (26.8 +/- 9.3%) but not different to that after 140 days gestation (29.9 +/- 5.5%). Between 110-117 days, cortisol infusion had no effect on the proportion of IR-ACTH in the LMW range (43.9 +/- 5.7%, saline infused; 44.1 +/- 2.4%, cortisol infused). Between 121-125 days, the proportion of IR-ACTH in the LMW range in the CRF-infused groups (with or without prior exposure to cortisol) was significantly lower (27.4 +/- 2.1%) than in the saline-infused control group. In contrast, after fetal adrenalectomy, the proportion of IR-ACTH in the LMW range between 126-139 days was significantly higher (48.0 +/- 6.7%) than in intact control animals (23.8 +/- 3.5%). We conclude that the change in the mol wt profile of IR-ACTH in fetal plasma after 125 days may be a consequence of changes in the morphological and/or functional characteristics of the corticotrophic cells in the fetal pituitary. Infusion of oCRF appears to accelerate the normal maturation of the fetal pituitary-adrenal relationship, and oCRF acting either directly or via secretion of cortisol may play a role in the posttranslational processing of POMC in the fetal sheep pituitary after 125 days gestation.

Adrenalectomy↗
PubMed1975

Bioactive and immunoactive ACTH in the rat pituitary: influence of stress and adrenalectomy.

Tissue levels of bioactive and immunoactive ACTH were measured in both the anterior and neuro-intermediate lobes of the rat pituitary. Similar concentrations of bioactive (65 ng/mg) and immunoactive (83 ng/mg) ACTH were found in the anterior lobes control rats. A 2-min ether stress had no effect on either bioactive or immunoactive ACTH levels in the anterior lobe. Twenty-four h after adrenalectomy the anterior lobe content of both bioactive and immunoactive ACTH decreased only to return to supranormal levels 21 days after the operation. A 30-min neurogenic stress had no effect on anterior lobe bioactive ACTH content but reduced the immunoactive ACTH level to 50 ng/mg. Synthetic alphah-17-39 ACTH was used in our radio-immunoassay in order to measure the C-terminal ACTH activity of the neuro-intermediate lobe. The concentration of such C-terminal activity in control rats (890 ng alphah-17-39 ACTH/mg) considerably exceeded the amount of bioactive ACTH (15 ng/mg). This is presumably due primarily to the presence of the so-called corticotropin-like intermediate lobe-peptide (CLIP). The amounts of bioactive or C-terminal immunoactive ACTH in the neuro-intermediate lobe were not affected by ether stress nor short term (24-h) or long term (21-day) adrenalectomy. Neuro-intermediate lobe bioactive ACTH decreased (to 8 ng/mg) only with the introduction of a 30-min neurogenic stress. Neurogenic stress had no effect on the concentration of CLIP, but when the stress was imposed 24 h after adrenalectomy, a significant reduction was observed. The data support the presence of bioactive ACTH in the intermediate lobe of the rat pituitary and suggest that such ACTH is preferentially released by neurogenic stress and not appreciably regulated by circulating levels of glucocorticoids. Until the biological function and/or target organ of CLIP is identified, the significance of the changes in tissue levels of C-terminal immunoactive ACTH will remain unknown.

Adrenal Glands↗
PubMed1999

Glucocorticoid replacement, but not corticotropin-releasing hormone deficiency, prevents adrenalectomy-induced anorexia in mice.

There is considerable evidence that CRH can suppress food intake. As hypothalamic CRH, a main site of CRH expression, is also negatively regulated by glucocorticoids, it is unclear whether anorexia and weight loss in adrenal insufficiency are attributable to elevated CRH or to decreased glucocorticoid levels. To distinguish these possibilities, we have measured food intake and body weight in wild-type and CRH-deficient mice after sham adrenalectomy (Sham ADX) or adrenalectomy (ADX) with and without corticosterone (B) replacement. CRH deficiency neither increased basal food intake and body weight nor attenuated decreases in food intake after ADX or Sham ADX. B replacement producing plasma levels above the circadian peak completely blocked ADX-induced decreases in feeding and body weight in all mice and frequently stimulated food intake in CRH-deficient mice. Plasma levels of insulin and leptin, two other hormones involved in appetite regulation, did not differ between genotypes; however, the relationship between food intake and circulating leptin was significantly less negative at B doses that preserved appetite. B replacement levels slightly below circadian peak concentrations did not prevent hypophagia after ADX. We conclude that factors other than or in addition to CRH are more important in mediating appetite responses to adrenalectomy.

Adrenalectomy↗
PubMed1995

The long-term outcome after adrenalectomy and prophylactic pituitary radiotherapy in adrenocorticotropin-dependent Cushing's syndrome.

We have reviewed our experience of adrenalectomy performed as part of the management of 56 patients with ACTH-dependent Cushing's syndrome between 1946 and 1993. Forty-three patients were operated on at our institution. Surgery-related mortality did not occur, but complications developed in 14 (33%); these were minor in 12. Eleven patients (29%) of the 38 for whom long-term follow-up data were available and who did not have a proven ectopic source of ACTH subsequently developed Nelson's syndrome, diagnosed on the basis of clinical pigmentation and markedly elevated ACTH levels that were not normally suppressible with glucocorticoids. The effects of prophylactic pituitary radiotherapy were assessed in 38 patients who underwent adrenalectomy at our institution and 18 who underwent surgery elsewhere. Patients who had received prophylactic radiotherapy were less likely to develop Nelson's syndrome (5 of 20, 25%) compared to those who did not (18 of 36, 50%; P > 0.07), and there was a low incidence of radiotherapy-induced hypopituitarism. We conclude that total adrenalectomy has proved to be a safe and effective operation and still may be indicated in selected patients with ACTH-dependent Cushing's syndrome; because prophylactic pituitary radiotherapy reduces the incidence of subsequent Nelson's syndrome by 50%, it should always be considered in the management of these patients.

Adolescent↗
PubMed1983

Characteristics of glucocorticoid-binding sites of rat liver: different effects of adrenalectomy on the binding.

Hydrocortisone (HC) in rat liver cytoplasmic fraction was bound to three different binding sites with high, medium and low affinity. Dissociation constants (Kd) were approx. 2.1, 22 and 208 nM; and the densities of these binding sites were about 40, 50 and 10% of total number of binding sites, respectively. The binding site for dexamethasone (DM) of the cytoplasmic fraction was the medium affinity one among these three components. The maximum number of binding sites (Bmax) of HC and DM was significantly increased by adrenalectomy. The Bmax of HC was about twice as great as that of DM in normal and adrenalectomized rat liver. DM inhibited 3H-HC binding in a dose-dependent manner but inhibition did not exceed 50% in either normal or adrenalectomized rats. Following adrenalectomy, the Bmax of the medium affinity-site for HC was significantly increased, while the high affinity component disappeared. By adding DM to the cytoplasmic fraction of adrenalectomized rat liver in vitro and in vivo, the Bmax of the medium affinity-site was significantly decreased, and a high affinity component of HC was revealed with a significant increase in the number of binding sites. These results indicate that the binding site for DM is one component of the HC binding site; and following adrenalectomy, the number of each type of binding site for glucocorticoids increases differently from the others.

Adrenalectomy↗
PubMed1996

Effect of maternal adrenalectomy and corticosterone therapy on the early development of B-cells in the fetal pancreatic islet in the rat.

Pregnant Wistar rats were divided into 3 groups, non-operated control, adrenalectomized, and adrenalectomized and corticosterone-treated. Maternal adrenalectomy was performed on day 6 of gestation. Corticosterone therapy was made from the day at operation to the day at observation. The growth pattern of insulin-producing B-cells was observed immunohistochemically and histometrically from days 12 to 16. The results obtained were as follows: From day 12 to day 15, maternal adrenalectomy resulted in a significant retardation of the growth of insulin-positive B-cells in terms of the collective volume of the cells. Maternal corticosterone therapy prevented this retardation. On day 16, however, the growth of B-cells in collective volume overcame the suppressive effect of maternal adrenalectomy. These results suggest that the lack of adrenocortical hormones causes a retardation of B-cell growth in early development, and that, when once developed well, B-cells can grow independently of the hormones.

Adrenalectomy↗
PubMed1993

Acromegaly with hyperprolactinemia developed after bilateral adrenalectomy in a patient with Cushing's syndrome due to adrenocortical nodular hyperplasia.

A 27-yr-old woman was referred for evaluation of acromegaly and hyperprolactinemia. She had undergone left adrenalectomy at 12 and right adrenalectomy at 17 for Cushing's syndrome due to adrenocortical nodular hyperplasia. At this time a pituitary tumor was found by brain computerized tomography, but plasma levels of growth hormone (GH), prolactin (PRL) and adrenocorticotropin (ACTH) were normal. When she was 23, symptoms and signs of acromegaly and subsequently galactorrhea-amenorrhea had developed. Plasma GH and PRL were increased and she was followed up by the administration of bromocriptine (2.5 mg-12.5 mg/day, p.o.). However the plasma GH level had been increasing gradually. On admission, plasma GH and PRL were high (19.5 micrograms/L, 61.0 micrograms/L, respectively) and increased in response to thyrotropin releasing hormone (TRH, 500 micrograms i.v.). An intrasella mass, which had been detected when she was 17, had become enlarged and was removed by Hardy's operation. Microscopically, the resected tumor was an eosinophilic adenoma. Immunohistochemical studies showed GH, PRL and ACTH positive cells localized in the tumor. Immunoultrastructural analysis of the tumor confirmed that GH, PRL and ACTH were present in secretory granules and Golgi apparatus in the tumor cells. The patient was a rare case of acromegaly with hyperprolactinemia developed after bilateral adrenalectomy of Cushing's syndrome due to adrenocortical nodular hyperplasia, all of which manifestations may be caused by a GH, PRL and ACTH secreting pituitary adenoma.

Acromegaly↗
PubMed2005

Adrenocorticotropin hypersecretion and pituitary microadenoma following bilateral adrenalectomy in a patient with classic 21-hydroxylase deficiency.

Bilateral adrenalectomy is an acceptable alternative treatment in salt-wasting 21-hydroxylase deficiency when conventional steroid replacement therapy fails to control hyperandrogenism. Objections to surgical adrenalectomy have been based on surgical risk, possible loss of protective adrenal function, and the risk of ACTH-induced activation of adrenal rest tissue. We report a young female with salt-wasting CAH, who underwent bilateral adrenalectomy and developed severe hyperpigmentation, progressively marked corticotropin hypersecretion to concentrations seen in Nelson's syndrome (5,000-7,000 pg/ml), a pituitary microadenoma 5 years postoperatively, and probable ectopic adrenal rest tissue. Corticotropin concentrations failed to respond to ovine corticotropin-releasing hormone (oCRH) (1 microg/kg given as an i.v. bolus), but did suppress following both hydrocortisone administration (100 mg given as an i.v. bolus) and a low dose (0.5 mg given orally every 6 h for 48 h) dexamethasone suppression test. Patients with CAH have hyperactivity of the hypothalamic-pituitary-adrenal axis and are at risk for pituitary tumor formation.

Adenoma↗
PubMed1982

Developmental patterns of levels of corticosterone and of corticosterone binding in the serum of female rats: effects of ovariectomy and adrenalectomy.

Corticosterone concentrations and corticosterone binding in the serum were studied in immature female rats, using radioimmunoassay and batchwise gel equilibrium techniques. A parallel developmental pattern was found for corticosterone levels and its serum binding with a neonatal drop, followed by low levels until 12 days of age and a rise between 12 and 28 days of age. Effects of adrenalectomy, of ovariectomy, of the combined operation and of sham-operations, performed at various ages, were also studied. Adrenalectomy performed at 5 days of age did not decrease serum corticosterone concentrations within a 6-day period whereas it did in older rats. Complete disappearance of corticosterone from the blood occurred only in adult rats after combined adrenalectomy/ovariectomy. Ovariectomy and sham-operations in the younger age groups (5-15 days) caused a gradual increase in corticosterone concentration with maximal values 6 days after operation or later. The response of corticosterone secretion to these operations became more moderate and quicker, i.e. more adult-like, at 28 days of age, the age where corticosterone concentrations in intact rats also seemed to reach a plateau at an adult-like level. Corticosterone binding changed only marginally after ovariectomy or sham-operations until 28 days of age, when an increase was induced by these operations. After adrenalectomy or combined adrenalectomy/ovariectomy, however, marked increases in serum binding of corticosterone were always seen. In summary: though a parallel developmental pattern of serum corticosterone levels and corticosterone binding was seen in the maturing rat, interference with the normal condition causes divergent responses in these two parameters. Moreover, the responses vary with maturational age.

Adrenalectomy↗
PubMed1998

Laparoscopic adrenalectomy: a report on 50 operations.

OBJECTIVE: To investigate the feasibility, safety and results of laparoscopic transperitoneal adrenalectomies performed with the patient supine, in patients affected by secreting and silent adrenal lesions. METHODS: Exclusion criteria were suspected adrenal primary malignancies. Fifty patients (33 women and 17 men; mean age 49.6 years, range 19-75 years) underwent 51 laparoscopic adrenalectomies (one bilateral). After complete endocrinological evaluation, computed tomography or magnetic resonance imaging, or a combination thereof, 14 non-secreting adenomas, 13 aldosterone-producing adenomas, 13 cortisol-producing adenomas, eight phaeochromocytomas (one bilateral), one androgen-secreting adenoma, and two metastases were considered eligible for adrenalectomy. In five patients, associated procedures were performed during surgery. RESULTS: The lesions ranged in size from 1.5 to 10 cm. There were no intraoperative complications and no blood transfusions were required. The postoperative course was uneventful and painless in all patients. Mean postoperative hospital stay was 2.5 days. In all hypertensive patients, significant improvement or cure of hypertension was observed at follow-up (mean 18 months). In patients with secreting adenomas, normalization of hormone concentrations was obtained after removal of the tumour. In six patients with incidentaloma, the exaggerated 17-hydroxyprogesterone response to ACTH disappeared after surgery. CONCLUSIONS: Secreting and non-secreting adrenal lesions were treated safely by laparoscopy. Relatively small incidentalomas and subclinical hormonally active tumours can be removed by laparoscopy. Early diagnosis enhances prevention and treatment.

Adolescent↗
PubMed1988

Effects of adrenalectomy on photoperiod-induced changes in release of luteinizing hormone and prolactin in ovariectomized ewes.

Finnish Landrace x Southdown ewes were ovariectomized (OVX) and subjected to daily photoperiods of 16L:8D (Group I) or 8L:16D (Group II) for 84 days. Ewes were then either adrenalectomized (ADX) (N = 5 for Group I; N = 4 for Group II) or sham ADX (N = 6 for Groups I + II). After surgery, ewes in Group I were subjected to 8L:16D for 91 days and 16L:8D for 91 days whereas ewes in Group II were exposed to 16L:8D for 91 days and 8L:16D for 91 days. Oestradiol implants were inserted into all ewes on Day 148. Sequential blood samples were taken at 28, 56, 91, 119, 147 and 168 days after surgery to determine secretory profiles of LH and prolactin. Photoperiod did not influence LH release in Group I in the absence of oestradiol. Although photoperiod influenced frequency and amplitude of LH pulses in Group II before oestradiol treatment, adrenalectomy did not prevent these changes in patterns of LH release. However, in Group II the increase in LH pulse amplitude during exposure to long days was greater (P less than 0.01) in adrenalectomized ewes than in sham-operated ewes. Mean concentrations of LH increased in ADX ewes on Days 91 (P = 0.07) and 119 (P less than 0.05). Adrenalectomy failed to influence photoperiod-induced changes in mean concentrations of LH, amplitude of LH pulses and frequency of LH pulses in the presence of oestradiol. Concentrations of prolactin were influenced by photoperiod. In Groups I and II concentrations of prolactin increased (P less than 0.01) after adrenalectomy, but the magnitude of this effect decreased over time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗