Search PubMed⌕ Search

Biomedical subjects

W Hansel

Publications and source records attributed to W Hansel.

At least 73 records · Page 4Linked to original sources
PubMed1985

A seven-day synchronization method for ewes using medroxyprogesterone acetate (MAP) and prostaglandin F2 alpha.

Estrous cycles of adult (n = 27), farm-flock, Suffolk ewes and Polypay range ewes (n = 224) were controlled with medroxyprogesterone acetate (MAP)-impregnated vaginal pessaries inserted (d 0) for 7 d in combination with prostaglandin F2 alpha (PGF2 alpha) injected on d 6. Descriptive criteria of the effects of this treatment regimen on endocrine characteristics of the estrous cycle were evaluated in the experiment with farm-flock ewes. The efficacy of this synchronization regimen on reproductive performance of range-bred ewes was tested in a second trial. Suffolk ewes bred at the second observed estrus after treatment to provide comparisons of cycle length between treated and control ewes. Polypay ewes were exposed to fertile rams at the controlled estrus. Eighty-nine percent of Suffolk ewes were in estrus within 3 d after pessary removal. All nonsynchronized Suffolk ewes (n = 24) were in estrus over a 21-d period. Estrous cycle lengths of treated ewes averaged 16.8 +/- .2 d. Plasma progesterone concentrations were similar for treated and control ewes during the luteal phase of the estrous cycle. Ninety-one percent of the range-bred, controlled ewes lambed. Sixty-two percent of these ewes lambed within 150 d after exposure to fertile rams compared with only 17% of nonsynchronized ewes (P less than .05). Lambing percentage was similar by 167 d for treated (87%) or control (88%) ewes. Lambs per ewe exposed averaged 1.68 and 1.80 for treated and nonsynchronized groups, respectively. These data indicate the effectiveness of this 7-d treatment method for control of the estrous cycle of ewes during the normal breeding season. Results further show that this treatment scheme has practical application for range breeding of ewes.

Animals↗
PubMed1984

Calcium-dependent, cyclic nucleotide-independent steroidogenesis in the bovine placenta.

Dispersed bovine placental cells (fetal cotyledon and maternal caruncle) were shown to synthesize progesterone. To determine if their steroidogenic activity could be modulated by a cyclic nucleotide-mediated process, we added luteinizing hormone, 8-bromoadenosine 3',5'-monophosphate, 8-bromoguanosine 3',5'-monophosphate, adenosine, or cholera toxin to dispersed cells from placentomes of 100-283 days gestational age and examined progesterone synthesis during 3-to 16-hr incubation periods. Net progesterone production, defined as the amount of progesterone released in excess of the zero-time cellular progesterone content, was determined by using a specific RIA. None of these agents significantly affected progesterone synthesis. In contrast, the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (MIX; 0.2-0.5 mM) caused a marked increase in progesterone formation. In time course studies it was found that MIX produced a 5-fold increase in progesterone production in 16 hr, with steroid production increasing linearly during this time. MIX also increased the conversion of exogenous pregnenolone to progesterone by placental cells. In view of the failure of cyclic nucleotide analogues and activators of adenylate cyclase to stimulate steroidogenesis, it was necessary to consider other modes of action of MIX. Since MIX is known to affect intracellular calcium translocation, we examined the effects of the calcium ionophore A23187 on progesterone formation. This drug enhanced progesterone formation and augmented the stimulatory effects of MIX. The stimulatory action of A23187 was not affected by cyclic nucleotide analogues. Our data suggest that progesterone synthesis in the bovine placentome is calcium dependent and cyclic nucleotide independent.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Prolongation of the bovine estrous cycle with a gonadotropin-releasing hormone analog.

A series of in vitro and in vivo experiments was conducted to determine the effects of gonadotropin-releasing hormone (GnRH) on bovine luteal function. Biosynthesis of progesterone by bovine luteal cells during a 2-h incubation was determined following addition of 0, 10, 20, 40, 80 and 100 ng GnRH. Synthesis of progesterone was significantly depressed only by the 100-ng dose of GnRH. Luteal cells were incubated with 0.1 and 1.0 microgram GnRH in the presence and absence of 0, 1, 2 and 5 ng bovine luteinizing hormone (LH). Again, only the highest dose of GnRH significantly depressed LH-stimulated production of progesterone. Three experiments were conducted to assess the effects of repetitively administered GnRH. In the first, twice daily intrauterine infusions of 100 micrograms GnRH on Days 12, 13 and 14 of the bovine estrous cycle was without effect on plasma concentrations of progesterone and the functional life span of the corpus luteum (CL). In the second experiment, 10 micrograms of a highly potent GnRH analog (GnRH-A) was injected subcutaneously four times daily on Days 9-12 of the estrous cycle. GnRH-A-treated heifers had longer (P less than 0.05) mean estrous cycle lengths (26.2 +/- 0.72 days) when compared to control heifers (20.25 +/- 0.25 days). Plasma concentrations of progesterone were higher in the GnRH-A-treated group on Days 9-13 and Days 15-22 of the estrous cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Induction of lymphopenia causes luteal dysfunction in cattle.

Studies were conducted to determine the effects of lymphopenia on reproductive function in heifers. Ten normally cycling heifers were injected with antilymphocyte serum (ALS) or normal horse serum (NHS) once daily between Days 3-6 or 9-17 of the estrous cycle. The ALS caused a significant reduction in circulating lymphocytes without affecting other blood cells. Concentrations of plasma progesterone were reduced (P less than 0.05) in heifers treated with ALS compared to NHS-treated heifers. The concentrations of circulating luteinizing hormone (LH) were also reduced in ALS-treated heifers. LH determinations in frequently collected blood samples showed that the number of LH pulses in the ALS-treated animals (1.4 +/- 0.4) was significantly (P less than 0.05) lower than NHS-treated controls (3.2 +/- 0.2). These studies suggest that immunosuppression caused by induction of lymphopenia causes luteal dysfunction in cycling heifers as a result of decreased pituitary LH secretion.

Animals↗
PubMed1984

Origin of different cell types in the bovine corpus luteum as characterized by specific monoclonal antibodies.

Specific monoclonal antibodies to granulosa and thecal cell surface antigens were produced and used to determine the contributions of theca and granulosa cells to the bovine corpus luteum (CL). Binding of each antibody was examined on collagenase-dispersed luteal cells from 18 cycling and 14 pregnant heifers by indirect immunofluorescence. The percent binding of the large luteal cells to granulosa antibody (GrAb) declined (P less than 0.01) as the age of the CL advanced: 77 +/- 6, 47.5 +/- 3, and 30 +/- 2 for Days 4-6, 10-12 and 16-18, respectively. Further reduction in binding of GrAb to large cells occurred between 50 and 100 days of pregnancy and no labeling was seen thereafter. Fourteen percent of the small luteal cells were bound by GrAb on Days 4-6 of the cycle, and none were labeled during subsequent stages. In contrast, when thecal antibody (TAb) was used, the proportions of large cells that were labeled increased (P less than 0.01) between Days 4-6 (10 +/- 1.3%) and 10-12 (46 +/- 3%). The percentage of large cells bound by TAb then remained unchanged until midpregnancy, declined as pregnancy advanced, and disappeared during late gestation. A majority of small luteal cells were bound by TAb throughout the estrous cycle: 70 +/- 4%, 69 +/- 3% and 58 +/- 6% at Days 4-6, 10-12, 16-18, respectively. Labeling of small cells by TAb occurred throughout pregnancy but declined (P less than 0.05) as gestation advanced. These studies suggest that the large cells of the early cyclic CL are derived from granulosa cells, while most of the small cells are of thecal origin. Small cells develop into large cells as the age of the CL increases. Granulosa-derived cells disappear during early pregnancy, while cells of thecal origin persist throughout pregnancy.

Animals↗
PubMed1984

Modulation of bovine placental prostaglandin synthesis by an endogenous inhibitor.

An endogenous, heat-labile, inhibitor of prostanoid synthesis in maternal caruncle tissue of bovine placentomes was studied. Inhibitory activity was present in caruncle extracts from days 120-250 of gestation, but was not detectable at term (260-280 days). The disappearance of inhibitory activity coincided with an increase in the secretion of prostanoids by dispersed caruncle cells in culture. Coculture of caruncle cells from placentomes of 120-day gestation with fetal cotyledon cells resulted in suppression of prostanoid synthesis by the cotyledon cells. However, this inhibition was not observed in cocultures of dispersed caruncle cells and fetal cotyledon cells from term placentomes. Our findings indicate that an endogenous inhibitor modulates bovine placental prostaglandin synthesis. A decline in the level of this inhibitor at term may be one factor triggering increased prostanoid synthesis required for parturition.

Animals↗
PubMed1984

Insemination of Holstein heifers at a preset time after estrous cycle synchronization using progesterone and prostaglandin.

Two experiments were conducted to study estrous cycle control regimens that combine progesterone administration via an intravaginal device ( PRID ) with a single injection of prostaglandin F2 alpha (PG). In Exp. I, 242 Holstein heifers were assigned randomly to one of three treatment groups at 14 to 18 mo of age. Treatments were: 1) control, 2) PRID -6 + PG-6 ( PRID in place for 6 d plus PG on the day of PRID removal) and 3) PRID -7 + PG-6 ( PRID in place for 7 d plus PG on the day before PRID removal). Heifers were observed for estrous activity and were inseminated at 8 to 20 h after estrus was detected. Estrus and ovulation were effectively synchronized after both PRID + PG treatments. Ninety-nine percent of the heifers in each group were in estrus within 168 h after PG injection. However, the interval from PG administration to the onset of estrus was longer after PRID -7 + PG-6 (75 +/- 2 h) than after PRID -6 + PG-6 (66 +/- 2 h). A lower variance in the interval from PG treatment to estrus was observed after PRID -7 + PG-6, suggesting that the 24 h delay in PRID withdrawal improved the synchrony of the onset of estrus. Pregnancy rates (72 to 82%) did not vary across treatment groups. Two-hundred seventy-four heifers were assigned to Exp. II. Treatments were 1) control, 2) 2 X PG (two injections of PG at an 11 d interval) and 3) PRID -7 + PG-6.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Methylation in bovine luteal cells as a regulator of luteinizing hormone action.

Experiments were conducted to determine if methylation is a part of the mechanism by which luteinizing hormone (LH) and epinephrine stimulate progesterone production by dispersed bovine luteal cells. Corpora lutea (CL) were collected from 24 Holstein heifers on Day 10 of the estrous cycle and dispersed with collagenase. Net progesterone accumulation, representing total progesterone synthesized by 10(6) cells during a 2-h incubation was determined. Cells from 7 CL were treated with 0 and 5 ng LH, in the presence and absence of methylation inhibitor, S-adenosyl-homocysteine (SAH, 1 mM). LH-stimulated progesterone production was inhibited (P less than 0.05) in the presence of SAH(209 +/- 19 vs. 119 +/- 7 ng/10(6) cells). In the absence of LH, progesterone production was unaffected (87 +/- 22 vs. 68 +/- 28) by SAH. Cells from 4 CL were treated with 10 micrograms epinephrine or 10 micrograms isoproterenol with and without SAH. Both epinephrine and isoproterenol-stimulated progesterone production was inhibited (P less than 0.05) by the presence of SAH (204 +/- 24 vs. 125 +/- 18 and 198 +/- 15 vs. 130 +/- 8). Progesterone production by cells from 4 CL was unaffected by the presence of SAH when treated with Medium 199 (M199) (75 +/- 32), 10 micrograms cholera toxin, which directly stimulates adenylate cyclase on the cytoplasmic side of plasma membranes (168 +/- 19), or 3 mM dibutyryl cAMP (210 +/- 40).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Bovine placentomes contain factors which decrease progesterone secretion.

We examined the effects of 20% ammonium sulfate precipitates from cytosolic extracts of whole placental tissue collected between 100-150 days of gestation on progesterone secretion by bovine granulosa cells and dispersed bovine luteal cells. These extracts produced a dose-dependent inhibition (23-92%) of progesterone synthesis by bovine granulosa cells. However, no inhibitory activity could be demonstrated in similarly prepared extracts from term placentae. Inhibitory activity could be extracted from both maternal caruncles and fetal cotyledons. In the presence of 2 mg/ml of maternal caruncle extract, basal progesterone secretion was dramatically reduced (90%), as was steroidogenesis in the presence of bovine lutenizing hormone (bLH) and 8 bromocyclic (Br)-cAMP. Moreover, coincubation of dispersed luteal cells and dispersed fetal or maternal placental cells from 100- to 150-day placentae produced a significant (50%) reduction in progesterone content of the medium. The addition of 2 mg/ml of caruncle or fetal cotyledon extract from 100- to 150-day placentae also produced 100% and 50% inhibitions, respectively, of progesterone secretion by dispersed placental cells. Thus, the inhibitory factor appears to be produced by cells of both the maternal and fetal placenta. It is heat-stable and not extractable by ether. The inhibitory substance eluted was two distinct peaks from Sephadex G-100 columns, one with a molecular weight of about 60,000 daltons and the other about 30,000 daltons. Using isoelectric focusing, several peaks of inhibitory activity were obtained, one with a pI of 3-5, the others having pIs between 6 and 9.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Prostacyclin, prostaglandin F2 alpha and progesterone production by bovine luteal cells during the estrous cycle.

Corpora lutea (CL) were collected from Holstein heifers on Days 5, 10, 15 and 18 (5/day) of the estrous cycle. Dispersed luteal cell preparations were made and 10(6) viable luteal cells were incubated with bovine luteinizing hormone (LH) and different amounts of arachidonic acid in the presence and absence of the prostaglandin (PG) synthetase inhibitor indomethacin. The concentrations of progesterone, PGF2 alpha and 6-keto-PGF1 alpha, the stable inactive metabolite of prostacyclin (PGI2), were measured. Day 5 CL had the greatest initial content of 6-keto-PGF1 alpha (1.01 +/- 0.16 ng/10(6) cells), and synthesized more 6-keto-PGF1 alpha (2.55 +/- 0.43) than CL collected on Days 10 (0.57 +/- 0.11), 15 (0.08 +/- 0.05) and 18 (0.19 +/- 0.03) during a 2-h incubation period. Arachidonic acid stimulated the production of 6-keto-PGF1 alpha by Days 10, 15 and 18 luteal tissue. PGF2 alpha was produced at a greater rate on Day 5 (0.69 +/- 0.17 ng/10(6) cells) than on Days 10 (0.06 +/- 0.01), 15 (0.04 +/- 0.02) and 18 (0.08 +/- 0.01). Arachidonic acid stimulated and indomethacin inhibited the production of PGF2 alpha, in most cases. The initial content of 6-keto-PGF1 alpha was higher than that of PGF2 alpha on all days of the cycle and more 6-keto-PGF1 alpha was synthesized in response to arachidonic acid addition. The ratio of 6-keto-PGF1 alpha content to PGF2 alpha content was 4.39, 2.30, 1.25 and 1.13 on Days 5, 10, 15 and 18, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Luteolytic effect of 13,14-dihydro-PGF-2 alpha in heifers.

Holstein heifers (4/group) were injected intramuscularly with 0, 5, 10 or 25 mg 13,14-dihydro-PGF-2 alpha on Day 10 of the oestrous cycle. Complete luteolysis and precocious oestrus occurred in 3 of 4 heifers receiving 25 mg and 1 of 4 receiving 10 mg 13,14-dihydro-PGF-2 alpha injected i.m. These features were not affected in heifers injected with 0 or 5 mg 13,14-dihydro-PGF-2 alpha, although plasma progesterone concentrations were depressed in all treated heifers within 75 min. LH concentrations were elevated between 5 and 8 h after 13,14-dihydro-PGF-2 alpha in all treated heifers. The addition of 13,14-dihydro-PGF-2 alpha to dispersed bovine luteal cells did not affect progesterone accumulation during a 2-h period. These results suggest that 13,14-dihydro-PGF-2 alpha may play a role in PGF-2 alpha-induced luteolysis.

Animals↗
PubMed1983

A luteolytic interaction between estradiol benzoate and prostaglandin F2 alpha in cattle.

A possible luteolytic interaction between prostaglandin F2 alpha (PGF2 alpha) and estradiol benzoate (E2B) in cattle was investigated by randomly assigning 20 heifers to one of four groups of a 2 x 2 factorially designed experiment. The treatments for the groups consisted of im administration of: 1) 200 micrograms of E2B, given twice daily on d 10, 11 and 12 of the estrous cycle plus 7 mg PGF2 alpha, given at a separate site, but concurrently with the last injection of E2B; 2) the vehicles for E2B (sesame oil) and PGF2 alpha (saline); 3) E2B and saline and 4) sesame oil and PGF2 alpha. Administration of both E2B and 7 mg PGF2 alpha resulted in luteolysis as evidenced by a shorter mean length of the estrous cycle (P less than .05) when compared with the vehicle-treated control group, and a decline in systemic concentrations of progesterone to less than 1 ng/ml in four of five animals. Administration of PGF2 alpha with sesame oil was luteolytic in only one of five animals and E2B plus saline had no effect on the mean length of the estrous cycle or systemic concentrations of plasma progesterone. These observations suggested a luteolytic interaction between E2B and PGF2 alpha. This luteolytic interaction was examined further in a second experiment. Corpora lutea was removed 12 h after treatment with 200 micrograms E2B or .5 ml sesame oil, administered twice on d 10, 11 and 12 of the cycle, and incubated with luteinizing hormone (LH) and PGF2 alpha in vitro. The effect of both LH and PGF2 alpha was to increase progesterone synthesis (P less than .01), and this effect was observed irrespective of E2B pretreatment. These findings were not consistent with the hypothesis that the luteolytic site of action for either E2B or PGF2 alpha was inhibition of the steroidogenic effects of LH as assessed under in vitro conditions.

Animals↗
PubMed1982

Luteolysis-induced changes in phase composition and fluidity of bovine luteal cell membranes.

X-ray diffraction, fluorescence polarization of trans-parinaric acid, and fluorescence photobleaching recovery of dioctadecyltrimethyneindolecarbocyanine have been used to characterize the phase composition and liquid phase fluidity of bovine luteal cell membranes and membrane lipids for functional corpora lutea collected at midcycle and for regressing corpora lutea collected after treatment with prostaglandin F2 alpha. These results support previous observations of gel phases in microsomal preparations of regressed luteal cells at physiological temperatures and further suggest that the plasma membrane may be the main source of this gel phase. Analysis of the overall lipid composition of the microsomal preparations from these cells indicates a role for sphingomyelin, in the presence of cholesterol, for the generation of a gel phase at physiological temperatures.

Animals↗
PubMed1982

Study of the direct action of luteinizing hormone-releasing hormone agonists at the testicular level in intact rats treated with an antiluteinizing hormone serum.

Is it well known that LHRH agonists can inhibit testicular functions by gonadal desensitization secondary to endogenous LH release and that a direct action at the gonadal level has also been demonstrated. Since an excess of anti-LH serum can be used, as an alternative to hypophysectomy, to neutralize the influence of endogenous LH release, the relative importance of the testis and pituitary gland in the inhibitory effect of a LHRH agonist, [D-Ser-(TBU)6,des-Gly-NH210]LHRH ethylamide (Buserelin), was studied on gonadal gonadotropin receptors in intact adult male rats treated with equine anti-LH or normal horse serum (NHS). A single administration of increasing doses (1-100 ng) of Buserelin leads to a progressive inhibition of testicular LH and PRL receptor levels by 70% and 40%, respectively, in animals injected with NHS. Treatment with the anti-LH serum completely prevents this inhibitory effect of a single dose of the LHRH agonist. After two successive injections of Buserelin in NHS-treated animals, testicular LH receptors are reduced by 70% and 80% with the 100- and 500-ng doses, respectively, while testicular PRL receptors are inhibited by 40-60%. In animals treated with the anti-LH serum, the inhibition of testicular LH receptors is reduced by only 18% (100 ng Buserelin) and 55% (500 ng Buserelin), while the inhibitory effect on PRL receptors is abolished. The present data show that endogenous LH release induced by a single injection of a LHRH agonist plays an essential role in the loss of testicular LH receptors measured 2 days later. Moreover, upon repeated injection of the LHRH agonist, neutralization of endogenous LH release by an anti-LH serum markedly reduces the inhibitory effect of the LHRH agonist on LH receptors, while it completely prevents the effect on PRL receptors, suggesting that the inhibitory effect of the LHRH agonist in the male rat is predominantly due to endogenous LH release rather than to a direct action of the peptide at the testicular level.

Animals↗
PubMed1982

Evidence of membrane changes during regression in the bovine corpus luteum.

Microsomal membranes prepared from bovine corpora lutea (CL) were examined by wide angle x-ray diffraction to determine if there were structural changes in the cellular membranes during regression. In samples prepared from CL removed at midcycle, all of the membrane lipid was in the liquid crystalline phase at body temperature. However, examination of microsomes prepared from regressing luteal tissue revealed a phase transition in which a portion of the lipid bilayer was in a gel phase at body temperature. Coincident with this physical change was a decline in CL function. These results indicate that there are structural changes that occur at the submicroscopic level in cellular membranes during luteal regression, which appear to be related to the loss in cellular function.

Animals↗