Search Results
You are looking at 1 - 10 of 50 items for
- Author: D. T. BAIRD x
- Refine by access: All content x
Search for other papers by D. T. BAIRD in
Google Scholar
PubMed
Prostaglandin F2α (PGF2α) has been shown to be luteolytic in sheep when infused into the ovarian artery in situ (Thorburn & Nicol, 1971) or when autotransplanted to the neck (McCracken, Glew & Scaramuzzi, 1970). It was originally suggested that PGF2α might induce luteal regression by causing venoconstriction in the utero-ovarian vein and hence an alteration in ovarian blood flow (Pharriss & Wyngarden, 1969). Variable changes in total ovarian blood flow have been described after intra-arterial infusion of PGF2α in sheep (McCracken et al. 1970; Chamley, Buckmaster, Cain, Cerini, Cerini, Cumming & Goding, 1972).
Prostaglandin F2α was infused into the ovary through the ovarian artery at a dose of 40 μg/h in nine experiments in four ewes with autotransplanted ovaries. Ovarian blood flow and progesterone secretion rate were measured, as previously described (Collett, Land & Baird, 1973), at intervals during and immediately after a 4 h infusion (Fig. 1).
Search for other papers by K. P. MCNATTY in
Google Scholar
PubMed
Search for other papers by D. T. BAIRD in
Google Scholar
PubMed
The concentrations of FSH, oestradiol and androstenedione in the follicular fluid of normal and cystic human follicles were measured at different stages of the menstrual cycle. In addition, the number of granulosa cells in the follicles was determined.
In follicles in which FSH was detectable, the concentration of oestradiol was greater than that of androstenedione, irrespective of the stage of the cycle. In contrast, in those follicles in which FSH was undetectable and in all cystic follicles irrespective of the level of FSH, the concentration of androstenedione was greater than that of oestradiol. In follicles containing FSH there was a highly significant linear correlation between the number of granulosa cells and the concentration of follicular oestradiol (P < 0·001).
It is suggested that in human ovaries up to 90% of the oestradiol in follicular fluid may originate from the granulosa cells.
Search for other papers by D. T. BAIRD in
Google Scholar
PubMed
Search for other papers by R. A. COLLETT in
Google Scholar
PubMed
SUMMARY
The response of the ovine corpus luteum to repeated infusions of luteinizing hormone (LH) or of human chorionic gonadotrophin (HCG) was tested in four ewes with the left ovary autotransplanted to the neck. Constant infusion for 1 h of either LH (100 or 1000 μg/h) or HCG (200 i.u./h) via the ovarian artery stimulated a temporary increase in secretion of progesterone which fell to control levels by 60 min. Ovarian blood flow increased progressively (P < 0·05) throughout the infusion of gonadotrophin in three of the five experiments. A second infusion of either gonadotrophin after a further control hour failed to stimulate progesterone secretion. These results suggest that ovine luteal tissue rapidly becomes refractory to the steroidogenic effect of LH in vivo.
Search for other papers by D. T. BAIRD in
Google Scholar
PubMed
Search for other papers by R. J. SCARAMUZZI in
Google Scholar
PubMed
SUMMARY
The secretion rates of oestradiol, androstenedione and progesterone and the peripheral plasma concentration of LH were measured in 12 ewes with ovarian autotransplants before and after luteal regression induced by a single intramuscular injection of a synthetic prostaglandin (PG) analogue, 16-aryloxyprostaglandin F2α (I.C.I. 80996). Luteal regression was followed by a fourfold rise in the basal concentration of LH and increased secretion of oestradiol. In five out of six ewes there was a discharge of LH with the peak occurring 36–78 h after the injection of the PG analogue. The secretion of oestradiol declined from 3·68± 1·08 to 0·33± 0·6 (s.e.m.) ng/min in the 24 h following the LH peak (P < 0·001). In the remaining six ewes in which progesterone was implanted subcutaneously 24 h after the injection of PG analogue, follicular development was suppressed as indicated by the low secretion of oestradiol and androstenedione. The basal concentration of LH fell to values similar to those observed during the luteal phase after the implant of progesterone. The secretion of androstenedione followed a similar pattern to that of oestradiol in those ewes which showed presumptive evidence of ovulation. These results suggest that progesterone reinforces the negative feedback effects of oestrogen in the ewe.
Search for other papers by A. S. McNeilly in
Google Scholar
PubMed
Search for other papers by D. T. Baird in
Google Scholar
PubMed
ABSTRACT
Changes in the plasma concentration of inhibin were measured by radioimmunoassay in ovarian venous blood collected at 10-min intervals for 5-h periods between 16 and 21 h and 40 and 45 h after cloprostenol-induced luteal regression in six Finn–Merino sheep. Episodes of inhibin secretion occurred with an interpulse interval of 66 ± 5 min in both stages of the follicular phase. These changes in inhibin were unrelated to pulses of LH or oestradiol. There was no relationship with plasma concentrations of FSH, which did not change in a pulsatile manner. These results suggest that the release of inhibin by the preovulatory follicle(s) occurs in a pulsatile manner and is under local control by unknown factors.
Journal of Endocrinology (1989) 122, 287–292
Search for other papers by D. T. BAIRD in
Google Scholar
PubMed
Search for other papers by M. GILES in
Google Scholar
PubMed
Search for other papers by F. COCKBURN in
Google Scholar
PubMed
SUMMARY
The PO2, PCO2, pH and oxygen content were measured in blood from the carotid artery, and jugular and ovarian veins of six sheep with cervical ovarian autotransplants. The PO2 in ovarian venous blood (56·0 ± 3·9 (s.e.m.) mmHg) was lower than that in carotid arterial blood (94·3 ± 8·3) but higher than that in jugular venous blood (43·4 ± 3·1). The oxygen content of ovarian venous blood was significantly higher than that of jugular venous blood. The high PO2 and oxygen content in ovarian venous relative to jugular venous blood together with the high blood flow suggests the possibility of arterio-venous shunts within the ovary or its vascular pedicle.
Search for other papers by T. A. Bramley in
Google Scholar
PubMed
Search for other papers by G. S. Menzies in
Google Scholar
PubMed
Search for other papers by D. T. Baird in
Google Scholar
PubMed
ABSTRACT
The effects of a number of analogues of gonadotrophin-releasing hormone (GnRH) on the binding of a radiolabelled GnRH agonist (GnRH-A; d-Ser(But)6, des Gly10]GnRH-ethylamide) to homogenates of human corpus luteum (CL) and rat pituitary tissue were compared. Specific binding was inhibited by GnRH and GnRH-like peptides only. Both the C-terminal amide and N-terminal region of the GnRH molecule were required for binding in both tissues. However, amino acid substitutions at position 6 markedly enhanced, and at position 8 markedly reduced, binding potencies in rat pituitary tissue compared with human CL binding sites. These results indicate that GnRH-binding sites of rat pituitary and human luteal tissue have a similar degree of specificity for GnRH-like peptides, and a similar requirement for both N- and C-terminal regions of the peptide, but that differences in specificity related to the mid-chain region of GnRH exist between human luteal and rat pituitary binding sites.
J. Endocr. (1985) 000, 000–000
Search for other papers by T. A. Bramley in
Google Scholar
PubMed
Search for other papers by D. Stirling in
Google Scholar
PubMed
Search for other papers by I. A. Swanston in
Google Scholar
PubMed
Search for other papers by G. S. Menzies in
Google Scholar
PubMed
Search for other papers by D. T. Baird in
Google Scholar
PubMed
ABSTRACT
The specific binding of 125I-labelled human chorionic gonadotrophin (hCG), human low-density lipoprotein (hLDL), human FSH (hFSH) and human prolactin (hPRL) to homogenates of human corpus luteum tissue was measured.
Specific binding of 125I-labelled hCG was dependent on the temperature and duration of incubation, was inhibited by divalent metal ions or chelating agents, and increased linearly with homogenate concentration. Recovery of bound hormone was more effective using Millipore filtration or polyethylene glycol precipitation compared with centrifugation alone. Binding of 125I-labelled hCG was inhibited specifically by low levels of hCG and human LH (hLH) but not by ovine LH or bovine LH. Incubation of human luteal tissue with ice-cold citrate buffer (pH 3) released more than 90% of specifically bound 125I-labelled hCG within 5 min. This treatment inactivated LH receptors, but did not affect the immunoactivity of hLH released, enabling the measurement of released hormone by radioimmunoassay.
Scatchard plots of binding of 125I-labelled LDL to human corpus luteum demonstrated a single class of binding sites. Binding was saturable, increased linearly with increasing concentration of homogenate, and was displaceable by low concentrations of unlabelled LDL.
Binding of 125I-labelled hPRL to human luteal homogenates was increased by Mg2+ and was specific for lactogenic hormones (human prolactin, human growth hormone and ovine prolactin). Binding of 125I-labelled hFSH was not dependent on divalent metal ion concentration (in marked contrast to hFSH binding to immature pig granulosa cell receptors) and was displaced by hFSH preparations but not by hPRL, ovine LH or hCG at 1 μg/ml.
These results establish optimal conditions and hormone specificities for the measurement of human luteal gonadotrophin and LDL receptors, and methods for the estimation of hLH/hCG endogenously bound to human corpus luteum tissue.
J. Endocr. (1987) 113, 305–315
Search for other papers by T A Bramley in
Google Scholar
PubMed
Search for other papers by D Stirling in
Google Scholar
PubMed
Search for other papers by G S Menzies in
Google Scholar
PubMed
Search for other papers by D T Baird in
Google Scholar
PubMed
Scottish Blackface ewes were synchronised in mid-breeding (November; group 1; n=12 ewes) or late-breeding season (March; group 2; n=16). Anoestrous ewes (May) were treated with progestagen sponges for 7 days and then given 250 ng GnRH 3-hourly for 24 h, 2-hourly for 24 h and hourly for a further 24 h (group 3; n=12). A second group of anoestrous ewes (group 4, n=19) received three bolus injections (30 μg) of GnRH at 90-min intervals without progestagen pretreatment. After ovulation, ewes were bled twice daily until slaughter (day 4 or day 12: oestrus=day 0). Mid-breeding season (group 1) and anoestrous ewes in group 3 formed ‘adequate’ corpora lutea (CL) with high plasma progesterone levels (3–4 ng/ml) maintained for at least 12 days, and responded in vivo to ovine LH (oLH) (10 μg) with a rise in plasma progesterone on day 11 (group 3, but not group 1, ewes also responded on day 3). CL minces from these ewes responded to human chorionic gonadotrophin (hCG) in vitro with a dose-dependent increase in progesterone secretion. Ewes in group 4 had a foreshortened luteal phase (8–10 days) and low plasma progesterone levels (~1 ng/ml), consistent with formation of inadequate CL. LH injection failed to induce a significant plasma progesterone increase. Furthermore, although progesterone secretion in vitro in response to maximally stimulating doses of hCG or dibutyryl cAMP (dbcAMP) was similar to that in adequate CL, the sensitivity of these CL to hCG (EC (effective concentration)50, 1 IU hCG/ml) was reduced 10-fold compared with adequate CL (EC50, 0.1 IU hCG/ml; P<0.01). Ewes that ovulated in the late breeding season (group 2) had high plasma progesterone, although levels began to decrease after day 10. Injection of oLH in vivo increased plasma progesterone. However, sensitivity to hCG in vitro (EC50, 0.5 IU hCG/ml) was intermediate between that of adequate luteal tissue (groups 1 and 3; EC50, 0.1 IU/ml) and that of group 4 ewes (EC50, 1 IU hCG/ml). Our data demonstrate a markedly reduced luteal sensitivity to LH in vivo and hCG in vitro in Scottish Blackface ewes with inadequate CL, and suggest that a similar loss of sensitivity to LH may occur in the late breeding season.
Search for other papers by D. T. Baird in
Google Scholar
PubMed
Search for other papers by B. K. Campbell in
Google Scholar
PubMed
Search for other papers by A. S. McNeilly in
Google Scholar
PubMed
ABSTRACT
An experiment was conducted to examine the effect of steroid-free ovine follicular fluid (oFF) on ovarian hormone secretion. Eight Merino × Finnish Landrace ewes in which the left ovary and vascular pedicle had been autotransplanted to a site in the neck were studied during the breeding season. Luteal regression was induced in all animals by injection of cloprostenol (100 μg, i.m.) on day 10 of the luteal phase. Four of the eight animals were treated with steroid-free oFF (3 ml, s.c.) in the early follicular phase, 24 and 36 h after injection of cloprostenol. Samples of both ovarian and jugular venous blood were collected at 4-h intervals from 20 h before until 96 h after injection of cloprostenol. Ovarian and jugular venous blood samples were also collected at 10-min intervals from 48 to 52 h after injection of cloprostenol to investigate the pattern of pulsatile secretion of ovarian hormones. Samples were assayed for oestradiol, androstenedione, testosterone and inhibin and the ovarian secretion rates calculated.
Both injections of oFF resulted in a fourfold increase in the concentration of inhibin in jugular venous plasma within 4–8 h of administration (P < 0·01) with concentrations remaining increased (P < 0·05) until 56 h after cloprostenol (32 h after the first oFF injection). Following oFF injection there was a profound (100%; P < 0·001) and prolonged decrease in the peripheral concentration of FSH until 60 h after cloprostenol at which time the concentration of FSH increased five- to sixfold (P < 0·001) to a peak lasting 24 h. In contrast to FSH, the concentration of LH in jugular venous plasma rose immediately following oFF treatment and continued to increase, exhibiting a profile similar to that described for FSH. No preovulatory LH surge was detected in any of the oFF-treated ewes while untreated ewes had an LH surge within 58·0±1·2 (s.e.m.) h. Within 8 h of the first injection of oFF the ovarian secretion rate of oestradiol, androstenedione and inhibin began to decline to reach a nadir of less than 1 ng/min within 32–36 h (56–60 h after cloprostenol; P < 0·01). Testosterone secretion, already barely detectable, did not change significantly following injection of oFF but remained low for 36 h following oFF and did not exhibit the increase observed over this period in controls. After injection of oFF the episodic secretion of oestradiol, androstenedione, testosterone and inhibin was markedly suppressed in spite of numerous pulses of LH. Re-establishment of inhibin, androstenedione and testosterone secretion began from around 36 h after injection of oFF and continued to increase for the remainder of the experimental period (P < 0·001). The re-establishment of oestradiol secretion, however, took until 60 h after oFF treatment (84 h after cloprostenol). This increase in ovarian hormone secretion was temporally related to the decrease in the concentration of FSH and LH in jugular venous plasma that was observed at the end of the experimental period.
We conclude that treatment of ewes with steroid-free oFF during the follicular phase of the oestrous cycle results in the immediate inhibition of the ovarian secretion of oestradiol, inhibin, androstenedione and testosterone. This effect can most probably be attributed to the depression in FSH that occurs following oFF injection, although the possibility exists that other factors present in oFF are acting directly on the ovary to inhibit follicular growth.
Journal of Endocrinology (1990) 127, 23–32
