Involvement of the Amygdala in the Ovarian Compensatory Hypertrophy Response

1972 ◽  
Vol 9 (4) ◽  
pp. 228-234 ◽  
Author(s):  
S.W. Smith ◽  
Irene E. Lawton
Keyword(s):  
Compensatory Hypertrophy ◽  
Ovarian Compensatory Hypertrophy

STEROID-INDUCED BLOCK OF OVARIAN COMPENSATORY HYPERTROPHY IN HEMICASTRATED FEMALE RATS

1964 ◽  
Vol 29 (3) ◽  
pp. 255-NP ◽  
Author(s):  
D. L. PETERSON ◽  
R. A. EDGREN ◽  
R. C. JONES
Keyword(s):  
Follicular Development ◽  
Compensatory Hypertrophy ◽  
Left Ovary ◽  
Female Rats ◽  
Corpora Lutea ◽  
Steroidal Hormones ◽  
Ovarian Compensatory Hypertrophy ◽  
Ovarian Size ◽  
The Right ◽  
Higher Doses

SUMMARY Removal of the right ovaries of 160–180 g. rats was followed in 2 weeks by a hypertrophy of 55 % of the left ovary. This postoperative growth was prevented by the administration of various natural and synthetic steroidal hormones, which were compared at daily doses estimated to produce a 100 % block of the hypertrophy. The following steroids, together with approximate ED 100, were studied: oestrone, 17·8 μg.; oestradiol-17β, 20·4 μg.; oestriol, 95·5μg.; norethynodrel, 72·5μg.; progesterone, 3630μg.;testosterone, 436 μg.; norethisterone, 479 μg.; norbolethone, 155 μg. At doses above ED 100 the natural oestrogens and norethynodrel produced a secondary cycle of ovarian growth, whereas the Δ4-3-oxosteroids depressed ovarian size further. Hemicastrated rats had histologically normal ovaries which contained larger numbers of corpora lutea than those of the intact controls. All compounds appeared to increase follicular development at the ED 100 level; the higher doses of the oestrogens and norethynodrel stimulated excessive luteinization, whereas the Δ4-3-oxosteroids inhibited luteal development and produced large vesicular and cystic follicles.

THE INFLUENCE OF THE UTERUS ON THE CORPUS LUTEUM-PITUITARY RELATIONSHIP IN THE RAT

1963 ◽  
Vol 43 (4) ◽  
pp. 521-538 ◽  
Author(s):  
Martin Silbiger ◽  
Irving Rothchild
Keyword(s):  
Corpus Luteum ◽  
Compensatory Hypertrophy ◽  
Uterine Weight ◽  
Uterine Tissue ◽  
Late Afternoon ◽  
Mild Degree ◽  
Ovarian Compensatory Hypertrophy ◽  
Cervical Stimulation ◽  
Stimulation Of ◽  
Intact Rats

ABSTRACT The mechanism through which hysterectomy increases the duration of pseudopregnancy in the rat was studied. The operation resulted in a mean increase in dioestrous length of 8.8 days, and an incidence of such prolongations of about 78% when it was done before the late afternoon of the 9th dioestrous day; from this time until the 12th dioestrous day, the incidence of prolonged pseudopregnancies fell to 40%. Normal oestrous cycles were resumed following the pseudopregnant cycle, and cervical stimulation of such rats resulted in pseudopregnancies, of which 77% were prolonged. Sham operations involving only a mild degree of uterine trauma resulted in a 29% incidence of prolonged pseudopregnancies, while increase in the amount of uterine tissue removed (up to one entire horn) increased the incidence to 60%. The homotransplantation of a pituitary to pseudopregnant rats at the time of hysterectomy did not increase the incidence of prolonged pseudopregnancies in the first postoperative cycle, but did increase the degree of prolongation slightly. The cycles of hysterectomized rats bearing pituitary homotransplants – when compared with those of intact rats bearing such transplants – showed a 46% increase in the incidence of all pseudopregnant cycles; 10% of such cycles were prolonged in the intact rats, and 44% in the hysterectomized rats. Ovarian compensatory hypertrophy occurred at a slightly slower rate in cyclic hysterectomized rats than in rats with intact uteri; in pseudopregnant rats, hysterectomy delayed the onset of ovarian compensatory hypertrophy until after the 15th dioestrous day, while in rats with intact uteri, the increase in weight of the remaining ovary began on the 9th dioestrous day. The pituitary folliculotrophic potency (measured by mouse uterine weight increase) of pseudopregnant hysterectomized rats did not increase until the 15th day, while in pseudopregnant rats with intact uteri this increase was seen by the 7th day, and was of greater extent. These results were discussed in terms of whether hysterectomy increased LTH secretion, or decreased the secretion of a pituitary luteolytic factor, probably LH; it was suggested that the results could be more readily accounted for by the second possibility.

Ovarian Compensatory Hypertrophy Following Unilateral Ovariectomy in the Suckled Sow

1986 ◽  
Vol 63 (2) ◽  
pp. 572-578 ◽  
Author(s):  
M. J. Martin ◽  
D. A. Redmer ◽  
J. J. Ford ◽  
R. K. Christenson ◽  
B. N. Day
Keyword(s):  
Compensatory Hypertrophy ◽  
Unilateral Ovariectomy ◽  
Ovarian Compensatory Hypertrophy

THE INFLUENCE OF ADRENALECTOMY AND CORTICOID REPLACEMENT ON OVARIAN COMPENSATORY HYPERTROPHY IN RATS

1964 ◽  
Vol 47 (3) ◽  
pp. 485-490 ◽  
Author(s):  
Richard A. Edgren ◽  
DeAnn L. Peterson
Keyword(s):  
Growth Response ◽  
Cellular Metabolism ◽  
Compensatory Hypertrophy ◽  
Ovarian Compensatory Hypertrophy ◽  
Shift Hypothesis

ABSTRACT Adrenalectomy abolished the ovarian compensatory hypertrophy that followed unilateral castration in rats. Maintenance of the animals with saline to drink or with injected cortisol or deoxycorticosterone restored the response. These data are interpreted as follows: the absence of cortical hormones disrupts cellular metabolism, probably at the level of the ovary, so that the ovary is not capable of a growth response to the increased gonadotrophin available after hemicastration. The data do not support the »pituitary shift« hypothesis of Selye (1950).

Sign in / Sign up

Export Citation Format

Share Document