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Biomedical subjects

D J Bolt

Publications and source records attributed to D J Bolt.

At least 55 records · Page 3Linked to original sources

Luteinizing hormone, follicle stimulating hormone and prolactin secretion in ewes and wethers after zeranol or estradiol injection.

Plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) were determined over a 24-h period using radioimmunoassay in sheep injected with corn oil (control) or various doses of zeranol or estradiol-17 beta. Injection of .333, 1 or 10 mg of zeranol caused dose-related increases (P less than .01) in plasma PRL (peak levels at 12 to 18 h) and LH (peak levels at 12 to 20 h) in ovariectomized ewes. Similarly, PRL and LH increased following doses of 33 or 100 microgram of estradiol. Before the LH surge, plasma LH levels were significantly depressed (4 to 8 h). Plasma FSH levels were significantly decreased 4 to 8 h after zeranol and estradiol injection. Slight surges of FSH were observed at times similar to those of LH, but the peak level was never greater than control levels. Injection of 1 mg of zeranol or 100 microgram of estradiol into wethers resulted in a 24-h pattern of PRL secretion not significantly different of LH concentration and significantly prolonged inhibition of FSH secretion. These results indicate similarities in the effects of zeranol and estradiol on anterior pituitary hormone secretion within groups of animals of the same sex or reproductive state. Differences in secretion and plasma concentrations of LH, FSH and PRL due to underlying sexual dimorphism are maintained and expressed even when animals are challenged with structurally different compounds of varying estrogenic potencies.

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Effect of suckling on postpartum changes in 13,14-dihydro-15-keto-PGF2 alpha and progesterone and induced release of gonadotropins in autumn-lambing ewes.

Postpartum changes in concentrations of 13, 14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) and progesterone and gonadotropin-releasing hormone (GnRH) induced release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in two experiments on suckled and nonsuckled autumn-lambing ewes. In both experiments, one group of ewes had lambs weaned on d 3 +/- .5 postpartum and was compared with a second group of ewes that suckled one lamb each. In Exp. 1, jugular blood samples were collected daily from the day after lambing until d 50 postpartum for assay of PGFM and progesterone. On d 21 +/- .5 postpartum, ewes (eight suckled and eight nonsuckled) received GnRH (100 micrograms), and LH and FSH were measured in blood samples collected over a 340 min period. In Exp. 2, jugular blood samples were collected from the day of lambing until d 22 +/- .6 postpartum for assay of PGFM and progesterone. Ewes (six suckled and seven nonsuckled) received GnRH (100 micrograms) on d 22 +/- .6 postpartum, and LH and FSH were quantified in blood samples taken over a 185 min period. The pituitary was removed from each ewe 190 min after GnRH for LH and FSH determinations. Postpartum changes in concentrations of PGFM and progesterone did not differ with suckling in either experiment. In both experiments PGFM concentrations were high on d 1 postpartum, but declined to basal values by d 11. The release of LH after GnRH in Exp. 1 was greater (P less than .001) in suckled than in nonsuckled ewes. In Exp. 2, LH release after GnRH was not affected by suckling, but in both experiments suckled ewes had a greater (P less than .01) release of FSH than did nonsuckled ewes. Pituitaries from suckled ewes contained more FSH (P less than .01) than pituitaries from nonsuckled ewes. The resumption of ovarian cyclicity in well-fed autumn-lambing ewes appeared to be neither altered by suckling nor limited by the ability of the pituitary to respond to GnRH.

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Changes in plasma estrogen, luteinizing hormone, follicle-stimulating hormone and 13,14-dihydro-15-keto-prostaglandin F2 alpha during blockade of luteolysis in pigs after human chorionic gonadotropin treatment.

An injection of human chorionic gonadotropin (HCG) or estrogen on d 12 of the estrous cycle delays luteolysis in the pig. In an experiment to determine if HCG stimulated estrogen secretion, 21 cyclic pigs received one of five different amounts of HCG-(A) 0, (B) 125, (C) 250, (D) 500 or (E) 1,000 IU-as a single, im injection in 2 ml of distilled water on d 12 of the estrous cycle. Blood was collected from the jugular vein immediately before HCG injection and once daily thereafter until d 20 of the estrous cycle. Plasma progesterone, estrogen (unconjugated) and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) were quantified for pigs in all groups; luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were quantified for pigs in groups A and E. The HCG injection exerted a dose-related increase on the mean interestrus interval (groups A, B, C, D and E were 20.5, 20.2, 22.5, 31.0 and 61.4 d, respectively) and on the delay of luteolysis as measured by mean plasma progesterone on d 16 (A, B and C vs D and E, respectively, 1.9, 1.2 and 10.4 vs 34.1 and 47.1 ng/ml; P less than .05). The HCG injection caused a transitory increase in plasma estrogen from d 12 (5 to 10 pg/ml before treatment) to d 15 (35.5 pg/ml, group D) and to d 16 (90.2 pg/ml, group E) before it decreased to preinjection levels on d 17 (group D) and 18 (group E).(ABSTRACT TRUNCATED AT 250 WORDS)

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Acute and chronic changes in adenohypophyseal hormone secretion in sheep during zeranol administration.

The effect of zeranol on circulating plasma concentrations of 5 adenohypophyseal (anterior pituitary gland) hormones was investigated in growing, castrated male sheep in 3 studies: after IM injection of 1 mg of zeranol (acute study), during a 6-week period after subcutaneous implantation of 12 mg of zeranol (chronic study), and during a 4-hour continuous IV infusion of gonadotropin-releasing hormone (Gn-RH) plus thyrotropin releasing hormone (TRH), 10 micrograms/hour. The sheep used in the chronic study (challenge study) were the same animals used in the 6-week implant study. Plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), thyroid-stimulating hormone (TSH), and growth hormone (GH) were measured by specific radioimmunoassay. Injection of zeranol resulted in a transient decrease in circulating LH and prolonged reduction in FSH concentrations during the 24-hour sampling period. Plasma concentrations of PRL, TSH, and GH in zeranol-injected and control animals were not different. Implantation of zeranol caused chronic reduction in plasma LH and FSH, an increase in PRL, and no change in plasma GH or TSH concentrations compared with values for control animals. In the challenge study, IV infusion of Gn-RH and TRH caused a significant increase in the concentration of each of the 5 hormones compared with preinfusion values, regardless of zeranol treatment. When the hormone-response profiles were compared between zeranol-treated and control sheep in this challenge study, only the LH response was different--being greater in zeranol-treated sheep. Generally, the administration of zeranol resulted in a more pronounced alteration in basal and stimulated secretion of reproductive hormones such as LH, FSH, and PRL than in GH or TSH, which are more commonly associated with growth and development.

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Reduction by human chorionic gonadotropin of the luteolytic effect of prostaglandin F2 alpha in ewes.

The ability of human chorionic gonadotropin (HCG) to reduce the luteolytic effect of prostaglandin (PGF2 alpha) was demonstrated in cycling ewes. As expected, treatment with 10 mg of PGF2 alpha alone on Day 10 of the estrous cycle exerted a potent negative effect on the function and structure of corpus luteum (CL) as indicated by reduced plasma progesterone, CL progesterone, and CL weight. However, the identical PGF2 alpha treatment failed to significantly reduce either luteal function or luteal weight when administered to ewes that were also treated with HCG on Days 9 and 10 of the estrous cycle. Treatment with HCG alone had a positive effect on CL as indicated by increased plasma progesterone, CL progesterone, and CL weight. Treatment with HCG did not render the CL totally insensitive to the negative effects of PGF2 alpha because plasma progesterone was reduced when the dose of PGF2 alpha was doubled. Whether CL regressed or continued to function after treatment with both HCG and PGF2 alpha appeared to depend upon a balance between the positive and negative effects of the two hormones.

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Measurement of phagocytosis of 32P-labeled Staphylococcus aureus by bovine leukocytes: lysostaphin digestion and inhibitory effect of cream.

A procedure to measure phagocytosis by blood and milk neutrophils was developed. One milliliter of heat-killed 32P-labeled Staphylococcus aureus ([32P]SA) (180-200 X 10(6) CFU), 1 ml of phosphate-buffered saline solution (PBSS), and 2 ml of serum, whole milk, skimmed milk, whey, or PBSS were incubated in duplicate for 60 minutes at 37 C. Isolated blood or milk nuetrophils (polymorphonuclear leukocytes (PMN), 25 X 10(6) cells/ml; 1 ml) were added and incubated at 37 C for 30 minutes. Unphagocytosed [32P]SA organisms were lysed by incubation with 5 ml of lysostaphin (10 U) at 37 C for 30 minutes, and the PMN and phagocytosed T2P]SA were removed by centrifugation. Radioactivity of the supernatant was determined in a scintillation spectrometer and was used in estimate the percentage of [32P]SA phogocytosed. With this procedure, 25 assays in duplicate could be conducted each day with an expected coefficient of variation between duplicates of 5.6%. Blood PMN phagocytosed 80, 44, 74, 72, and 11% of the [32P]SA when incubated in serum, whole milk, skimmed milk, whey, and PBSS, respectively. Mik PMN phagocytosed 78, 44, 72, 74, and 22%, respectively. The addition of cream to either skimmed milk or serum reduced phagocytosis of [32P]SA by both blood and milk PMN. The inhibitory effect of cream was verified by the microscopic observation that PMN containing large quantities of ingested fat contained fewer S aureus. Seemingly, PMN upon entering the alveoli of the mammary gland become less efficiently phagocytic for bacteria, because of the presence of milk fat globules. This phef intramammary infection by invading mastitic pathogens.

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