Initiation of lactation in rats by nonspecific stresses

1960 ◽  
Vol 198 (5) ◽  
pp. 1103-1106 ◽  
Author(s):  
Charles S. Nicoll ◽  
P. K. Talwalker ◽  
Joseph Meites
Keyword(s):  
Anterior Pituitary ◽  
Corn Oil ◽  
Virgin Female ◽  
Mammary Glands ◽  
Female Rats ◽  
Common Mechanism ◽  
Duct System ◽  
Once Daily ◽  
Intense Light

Sixty mature, virgin female rats were divided into six groups of 10 each and injected subcutaneously for 10 days with 10 µg estradiol in 0.1 cc corn oil. For the following 5 days the groups were treated as follows: 1) controls, 0.1 cc saline injected subcutaneously once daily; 2) severe cold (0°C) 24 hr/day; 3) intense light and heat for 12 hr/day; 4) restraint, 12 hr/day; 5) starvation, no food or water for 5 days; 6) subcutaneous injection of 0.1 cc or 0.2 cc of 10% formaldehyde once daily. The mammary glands of the control rats regressed from a lobulo-alveolar system to a bare duct system during the period of saline injections. The stressed groups all showed variable degrees of lactation after treatment. It is concluded that nonspecific stresses can promote the secretion of prolactin and ACTH from the anterior pituitary in amounts adequate to induce lactation in estrogen-primed rats. The possible role of stresses in initiating lactation at parturition and under other circumstances is considered, and a common mechanism controlling the secretion of ACTH and prolactin is postulated.

Basal Lamina Formation in DMBA Induced Mammary Carcinoma

1977 ◽  
Vol 35 ◽  
pp. 534-535
Author(s):  
I. Russo ◽  
J. Saby ◽  
J. Russo
Keyword(s):  
Mammary Carcinoma ◽  
Virgin Female ◽  
Mammary Glands ◽  
Sesame Oil ◽  
Female Rats ◽  
Ultrastructural Changes ◽  
Post Inoculation ◽  
Intermediate Type ◽  
Sprague Dawley ◽  
Intercellular Spaces

It has been previously demonstrated that DMBA-induced rat mammary carcinoma originates in the terminal end bud (TEB) of the mammary gland by proliferation of intermediate type cells (1). The earliest lesion identified is the intraductal proliferation (IDP), which gives rise to intraductal carcinomas. These evolve to cribriform, papillary and comedo types (2). In the present work, we report the ultrastructural changes that take place in the IDP for the formation of a cribriform pattern.Fifty-five-day-old Sprague Dawley virgin female rats were inoculated intra- gastrically with 20 mg 7,12-dimethylbenz(a)anthracene (DMBA) in 1 ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from both control and experimental rats were removed weekly from the time of inoculation until 86 days post-inoculation. The glands were fixed and processed for electron microscopy (2).The first change observed in IDP's was the widening of intercellular spaces and the secretion of an electron dense material into these spaces (Fig. 1).

The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

1984 ◽  
Vol 42 ◽  
pp. 204-205
Author(s):  
I.C. Murray
Keyword(s):  
Mammary Gland ◽  
Dopamine Agonist ◽  
Alveolar Epithelium ◽  
Mammary Glands ◽  
Female Rats ◽  
Control Group ◽  
Cell Hyperplasia ◽  
Once Daily ◽  
Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

scholarly journals Chronic vasodilation increases renal medullary PDE5A and α-ENaC through independent renin-angiotensin-aldosterone system pathways

2013 ◽  
Vol 305 (10) ◽  
pp. R1133-R1140 ◽  
Author(s):  
Crystal A. West ◽  
Stefan Shaw ◽  
Jennifer M. Sasser ◽  
Andrea Fekete ◽  
Tyler Alexander ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Enzyme Inhibitor ◽  
Virgin Female ◽  
Normal Pregnancy ◽  
Female Rats ◽  
Plasma Volume Expansion ◽  
Renin Angiotensin Aldosterone System ◽  
Α Subunit ◽  
Renin Angiotensin

We have previously observed that many of the renal and hemodynamic adaptations seen in normal pregnancy can be induced in virgin female rats by chronic systemic vasodilation. Fourteen-day vasodilation with sodium nitrite or nifedipine (NIF) produced plasma volume expansion (PVE), hemodilution, and increased renal medullary phosphodiesterase 5A (PDE5A) protein. The present study examined the role of the renin-angiotensin-aldosterone system (RAAS) in this mechanism. Virgin females were treated for 14 days with NIF (10 mg·kg−1·day−1 via diet), NIF with spironolactone [SPR; mineralocorticoid receptor (MR) blocker, 200–300 mg·kg−1·day−1 via diet], NIF with losartan [LOS; angiotensin type 1 (AT1) receptor blocker, 20 mg·kg−1·day−1 via diet], enalapril (ENAL; angiotensin-converting enzyme inhibitor, 62.5 mg/l via water), or vehicle (CON). Mean arterial pressure (MAP) was reduced 7.4 ± 0.5% with NIF, 6.33 ± 0.5% with NIF + SPR, 13.3 ± 0.9% with NIF + LOS, and 12.0 ± 0.4% with ENAL vs. baseline MAP. Compared with CON (3.6 ± 0.3%), plasma volume factored for body weight was increased by NIF (5.2 ± 0.4%) treatment but not by NIF + SPR (4.3 ± 0.3%), NIF + LOS (3.6 ± 0.1%), or ENAL (4.0 ± 0.3%). NIF increased PDE5A protein abundance in the renal inner medulla, and SPR did not prevent this increase (188 ± 16 and 204 ± 22% of CON, respectively). NIF increased the α-subunit of the epithelial sodium channel (α-ENaC) protein in renal outer (365 ± 44%) and inner (526 ± 83%) medulla, and SPR prevented these changes. There was no change in either PDE5A or α-ENaC abundance vs. CON in rats treated with NIF + LOS or ENAL. These data indicate that the PVE and renal medullary adaptations in response to chronic vasodilation result from RAAS signaling, with increases in PDE5A mediated through AT1 receptor and α-ENaC through the MR.

Role of the Anterior Pituitary in the Development of a Fatty Liver

1958 ◽  
Vol 193 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Ira G. Wool ◽  
M. S. Goldstein
Keyword(s):  
Fatty Liver ◽  
Lipid Accumulation ◽  
Anterior Pituitary ◽  
Physiological Role ◽  
Female Rats ◽  
Hepatic Lipids ◽  
Hypophysectomized Rats

This study was undertaken to determine whether a fat mobilizing factor from the anterior pituitary is essential to the development of a fatty liver. The method employed was the administration of ethionine, an antimetabolite of methionine, to fasted female rats. Hypophysectomy led to a marked impairment in the ability to accumulate hepatic lipids. Cortisone alone or combined with thyroxine failed to restore this defect. Epinephrine administered to cortisone-maintained hypophysectomized rats led to the development of a fatty liver. While lipid accumulation in the liver can precede in the absence of a specific anterior pituitary fat mobilizing factor, the quantitative aspects do not exclude a possible physiological role for such a principle.

The Ultrastructural Basis For Increased Prolactin Synthesis and Release From Anterior Pituitary Glands of Estrogen-Progesterone Primed Ovariectomized Rats: Correlated Electron Microscopy and Radioimmunoassay

1973 ◽  
Vol 31 ◽  
pp. 564-565
Author(s):  
P. W. Coates ◽  
C. A. Blake ◽  
D. S. Maxwell ◽  
C. H. Sawyer
Keyword(s):  
Anterior Pituitary ◽  
Elevated Serum ◽  
Virgin Female ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Electron Microscopic ◽  
Pituitary Glands ◽  
Prolactin Synthesis

In rats, physiological studies show that ovariectomy results in a reduced concentration of circulating prolactin. Conversely, ovariectomized rats given estrogen have elevated serum prolactin and increased amounts of prolactin in the anterior pituitary gland. Separate electron microscopic studies suggest modifications in fine structure of prolactin producing (LTH) cells based on relatively large cumulative amounts of estrogen given alone or with comparably high doses of progesterone to adult virgin female or ovariectomized rats. This study was undertaken to provide a correlated morphological and physiological investigation of LTH cells and prolactin levels in a model commonly used by many researchers.Six to seven weeks after bilateral ovariectomy, a group of adult female rats was primed by a subcutaneous injection of 50 ng of estradiol benzoate and 25 mg of progesterone.

EFFECT OF PROLACTIN INHIBITORY AGENTS ON THE ECTOPIC ANTERIOR PITUITARY AND THE MAMMARY GLAND IN RATS

1977 ◽  
Vol 85 (2) ◽  
pp. 267-278 ◽  
Author(s):  
K.-J. Gräf ◽  
R. Horowski ◽  
M. F. El Etreby
Keyword(s):  
Mammary Gland ◽  
Anterior Pituitary ◽  
Direct Action ◽  
Mammary Glands ◽  
Female Rats ◽  
Simultaneous Administration ◽  
Dopaminergic Receptors ◽  
Oestradiol Benzoate ◽  
Biological Effectiveness ◽  
Inhibitory Agents

ABSTRACT The purpose of the present study was to investigate the biological effectiveness of two highly potent prolactin (PRL) inhibitors, lisuride hydrogen maleate (LMH) and 2-Br-α-ergocryptine (CB-154), in the absence of hypothalamic factors acting directly at the level of the anterior pituitary. Hypophysectomized female rats bearing 4 transplanted pituitaries beneath the kidney capsules were treated with oestradiol benzoate (OeB) and progesterone (P) with or without simultaneous administration of LHM or CB-154 for 22 days in order stimulate or inhibit lobulo-alveolar growth of the mammary glands. In addition to the investigation of the mammary glands by DNA determination and assessment of the histological pictures, the aim of this study was directed towards the influence of the substances tested at the level of the anterior pituitary remote from the hypothalmus. In this connection the changes in the different cells within the ectopic pituitaries as revealed by immunoenzyme-cytochemical studies were investigated. The results obtained support the classical view of a neuroendocrine regulation of mammary gland growth and the importance of oestrogens, P and PRL within this system. Both ergot derivatives LHM and CB-154 were able to antagonize the stimulatory effect of OeB combined with P on the mammary gland. With regard to the mechanism of action of LHM and CB-154 it is concluded that both substances act via a direct action on dopaminergic receptors within the ectopic anterior pituitary.

scholarly journals Induction of experimental mammary carcinogenesis in rats with 7,12-dimethylbenz(a)anthracene

2004 ◽  
Vol 59 (5) ◽  
pp. 257-261 ◽  
Author(s):  
Alfredo Carlos S. D. Barros ◽  
Elisa Naomi K. Muranaka ◽  
Lincon Jo Mori ◽  
Christina Helena T. Pelizon ◽  
Kyoshi Iriya ◽  
...  
Keyword(s):  
Animal Model ◽  
Light Microscopy ◽  
Breast Tumor ◽  
Mammary Carcinogenesis ◽  
Mammary Glands ◽  
Female Rats ◽  
Histopathological Analysis ◽  
Breast Carcinomas ◽  
Sprague Dawley

PURPOSE: To test an experimental model of chemical mammary carcinogenesis induction in rats. METHODS: Twenty young virgin Sprague-Dawley female rats, aged 47 days, received 20 mg of 7,12-dimethylbenz(a)anthracene (DMBA) intragastrically by gavage. Afterwards, at 8 and 13 weeks, their mammary glands were examined. At the end of the experiment, the animals were sacrificed, and the mammary tumors were measured and weighed. Tumor fragments were analyzed using light microscopy. RESULTS: Eight weeks after DMBA injection, 16 rats presented at least 1 breast tumor (80%). After 13 weeks, all of them (100%) developed breast carcinomas that were confirmed by histopathological analysis. CONCLUSION: This experimental animal model of chemical mammary induced carcinogenesis is feasible and can be used in further experiments on the role of tumorigenic biomodulator substances.

EFFECT OF OVINE LUTEINIZING HORMONE ON THE SECRETION OF PROGESTERONE IN VITRO BY OVARIAN FOLLICLES FROM HYPOPHYSECTOMIZED RATS TREATED WITH FOLLICLE-STIMULATING HORMONE

1978 ◽  
Vol 77 (3) ◽  
pp. 419-420
Author(s):  
A. R. LABARBERA ◽  
MERO R. NOCENTI
Keyword(s):  
New York ◽  
Luteinizing Hormone ◽  
Corn Oil ◽  
Follicle Stimulating Hormone ◽  
Virgin Female ◽  
Ovarian Follicles ◽  
Female Rats ◽  
Hypophysectomized Rats ◽  
Stimulating Hormone

Department of Physiology, College of Physicians and Surgeons, Columbia University, New York 10032, U.S.A. (Received 14 November 1977) Ovarian follicles from oestrous, pro-oestrous and hypophysectomized rats have the capacity to secrete progestins in vitro and to respond to luteinizing hormone (LH) by increasing this secretion (Stoklosowa & Nalbandov, 1972; LaBarbera, Nocenti & Castellano, 1974; Lindner, Tsafriri, Lieberman, Zor, Koch, Bauminger & Barnea, 1974). Follicles from hypophysectomized rats, untreated or treated with follicle-stimulating hormone (FSH), were therefore studied in experiments in vitro to investigate further the gonadotrophic control of progesterone secretion. Mature virgin female rats (200–250 g) were hypophysectomized and, beginning on day 4 after the operation, received a total of 360 μg ovine FSH (NIH-FSH-S9)/100 g body weight, injected s.c. in corn oil as six divided doses, one every 12 h for 3 days. Untreated controls received corn oil only. On day 7 after hypophysectomy, the ovaries were excised and

ROLE OF OESTROGENS AND GONADOTROPHINS IN PERPHENAZINE-INDUCED MAMMOGENESIS

1970 ◽  
Vol 48 (3) ◽  
pp. 365-371 ◽  
Author(s):  
A. DANON ◽  
C. P. WELLER ◽  
F. G. SULMAN
Keyword(s):  
Median Eminence ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Gonadotrophin Secretion

SUMMARY Treatment of intact or recently (1 day) ovariectomized female rats with 5 mg perphenazine (Trilafon)/kg/day for 5 days resulted in marked lobulo—alveolar differentiation of the mammary glands. Perphenazine failed to stimulate mammogenesis in chronically (12 days) ovariectomized rats, unless they had been primed with oestradiol. However, mammogenic effects in chronically ovariectomized rats were obtained after implantation of minute amounts (2 μg) of oestradiol into the median eminence, or after treatment for 16 days with the non-steroid pituitary gonadotrophin-inhibitor methallibure (ICI 33828; 20 mg/kg/day). Since these latter procedures counteract the gonadotrophin surge after ovariectomy, it would appear that inhibition of gonadotrophin secretion is necessary before prolactin secretion can be stimulated by perphenazine. Castrated male rats responded to perphenazine with lobulo—alveolar differentiation similar to that in intact males. The implications of this difference with regard to the mechanism of pituitary response to gonadectomy are discussed.

Modeling of fibrocystic mastopathy in experiment on animals

2020 ◽  
Vol 28 (4) ◽  
pp. 429-436
Author(s):  
Svetlana A. Anisimova ◽  
Janna A. Svirina ◽  
Denis A. Maksaev
Keyword(s):  
Mammary Gland ◽  
Virgin Female ◽  
Mammary Glands ◽  
Female Rats ◽  
Fibrocystic Disease ◽  
Drug Induced ◽  
Fibrocystic Mastopathy ◽  
Hormonal Imbalance ◽  
Pathogenetic Factor ◽  
Almost All

Nowadays, hormonal imbalance is proven to be a factor that influences initiation of malignant and benign breast tumors. To study the aspects of participation of sex hormones in damage to organs and tissues, it may be necessary to model a common womens pathology fibrocystic disease of mammary glands characterized by the most pronounced effects of this pathogenetic factor, on experimental animals. Aim. To create a model of fibrocystic disease of mammary gland with the subsequent possibility of studying morphological manifestations of the disease in natural and drug-induced pathomorphism. Materials and Methods. The pathology was induced by intramuscular injection of 0.5 ml of 2% synestrol and 0.5 ml of 2.5% progesterone to virgin female rats on the 1st, 7th, 14th, 21st, 28th and 35th days of the experiment. For examination, histological preparations of inguinal mammary glands were made. The preparations were described and studied using morphometric analysis. Results. In the result of the experiment, pronounced macro- and microscopic alterations of mammary glands were found. Microscopic picture was similar to that observed in fibrocystic mastopathy in women. Almost all the morphometric parameters underwent reliable alterations in correspondence with the given pathology. Conclusion. A model of fibrocystic disease of mammary gland was obtained that may be used for further study of morphogenesis and methods of correction.

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