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Biomedical subjects

C R Barb

Publications and source records attributed to C R Barb.

At least 91 records · Page 5Linked to original sources
PubMed1989

Luteinizing hormone secretion in hypophysial stalk-transected pigs given progesterone and pulsatile gonadotropin-releasing hormone.

This study was conducted to determine whether progesterone inhibits luteinizing hormone (LH) secretion in female pigs by a direct action on the pituitary gland. Eight ovariectomized, hypophysial stalk-transected gilts were given 1-microgram pulses of gonadotropin-releasing hormone iv every 45 min from Day 0 to 12. On Days 5-12, each of four gilts received either progesterone or oil vehicle im at 12-hr intervals. Serum progesterone concentrations in steroid-treated gilts reached 70 +/- 6.8 ng/ml (mean +/- SE) by Day 8 and remained elevated thereafter, whereas serum progesterone concentrations in oil-treated controls were less than 1 ng/ml for the entire study. Daily serum LH concentrations were not different between gilts treated with progesterone or oil. The 1-microgram pulses of gonadotropin-releasing hormone reliably evoked pulses of LH in both treatment groups. The LH pulse frequency and amplitude, assessed from samples collected every 15 min for 6 hr on Day 12, were similar for progesterone- and oil-treated gilts. These results provide evidence that progesterone does not act at the pituitary gland to alter LH secretion in pigs.

Animals↗
PubMed1988

On the site of action of naloxone-stimulated cortisol secretion in gilts.

The increase in serum cortisol concentrations following naloxone administration to female pigs was abolished by hypophysial stalk-transection, even though CRH and ACTH stimulated cortisol release in these animals. We suggest that the opioid antagonist enhances cortisol secretion primarily by a central action in pigs.

Adrenocorticotropic Hormone↗
PubMed1988

Absence of brain opioid peptide modulation of luteinizing hormone secretion in the prepubertal gilt.

Three experiments were conducted to evaluate the role of endogenous opioid peptides (EOP) in modulating luteinizing hormone (LH) secretion in the prepubertal gilt. In Experiment I, 8 prepubertal (P) gilts, 160-170 days of age (puberty = 197 +/- 10 days), received either 1 (n = 2), 3 (n = 3), or 6 (n = 3) mg/kg BW of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected by jugular vein cannula every 15 min for 2 h before and 2 h after NAL. All doses of NAL failed to alter serum LH concentrations. In Experiment II, 21 P gilts 160-170 days of age and 21 mature (M) gilts were ovariectomized (OVX). At the time of OVX, gilts were classified as prepubertal if their ovaries were devoid of corpora albicantia and corpora lutea. Three weeks after OVX, P and M gilts were injected twice daily for 10 days with either 0.85 mg/kg BW of progesterone (P4) or oil vehicle (V), resulting in the following groups: PP4 (n = 11), PV (n = 10), MP4 (n = 11), and MV (n = 10). All gilts received 1 mg/kg BW of NAL on the last day of treatment. Blood samples were collected via a jugular cannula every 15 min for 4 h before and 2 h after NAL treatment. NAL treatment resulted in an increase (p less than 0.05) in serum LH concentrations only in the MP4 gilts. In Experiment III, 15 OVX gilts 280 days of age were used. Ten of the 15 gilts were OVX prior to puberty at 160 days of age and were classified as chronologically mature (CM) at the time of treatment. The remaining 5 gilts were OVX after puberty, and were classified as sexually mature (SM) at the time of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Luteinizing hormone receptor number and affinity in corpora lutea from prepuberal gilts induced to ovulate and spontaneous corpora lutea of mature gilts.

This study was designed to determine if luteal cell receptors for luteinizing hormone/human chorionic gonadotropin (LH/hCG) contribute to the previously demonstrated abnormal function of induced corpora lutea (CL) in gilts. Twenty-five prepuberal (P) gilts, induced to ovulate with 1,500 IU pregnant mare serum gonadotropin followed 72 h later with 500 IU hCG (d 0 = day of hCG), and 22 mature (M) gilts that had displayed two or more estrous cycles were ovariectomized (OVX) on d 10, 14, 18, 22 or 26 after the onset of estrus. All gilts except those OVX on d 10 were hysterectomized between d 6 and 9 to ensure luteal maintenance. The CL were stored at -196 degrees C until determination of LH/hCG receptor number and dissociation constant (KD) by saturation analysis. Receptor number was greater for M than for P gilts on d 14 (P less than .07) and d 18 (P less than .01). The KD was greater in M than in P gilts on d 14 (P less than .01) and d 18 (P less than .0001). The LH/hCG receptor number and KD of P gilts remained the same throughout the days studied. The LH/hCG receptor number (fmol/mg protein) of M gilts was elevated on d 10, 14, and 18 (50.8, 50.4 and 51.4, respectively) and decreased on d 22 (26.5) and d 26 (25.4) to values similar to those of P gilts. In M gilts, KD increased on d 14, remained high on d 18 and decreased on d 22. We suggest that abnormal function of induced CL in P gilts may be due to an elevated LH receptor number.

Animals↗
PubMed1986

Opioid inhibition of luteinizing hormone secretion in the postpartum lactating sow.

Twelve lactating sows were used at 22.4 +/- 0.8 days postpartum to determine whether endogenous opioid peptides (EOP) are involved in the suckling-induced inhibition of luteinizing hormone (LH) secretion. Four sows each received either 1, 2, or 4 mg/kg body weight of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. All sows were then given 100 micrograms gonadotropin-releasing hormone (GnRH) in saline i.v., and blood samples were collected for an additional h. Pigs were weaned after blood sampling. At 40 h after weaning, sows were treated and blood samples collected as during suckling. Serum concentrations of LH after treatment with NAL were similar for all doses; therefore, the data were pooled across doses. During suckling, serum concentrations of LH were 0.41 +/- 0.04 ng/ml before NAL treatment, increased to 0.65 +/- 0.08 ng/ml at 30 min after NAL treatment, and remained elevated above pretreatment concentrations for 120 min (p less than 0.05). Naloxone failed to alter serum concentrations of LH after weaning. These data indicate that EOP may be involved in the suckling-induced suppression of LH secretion and that weaning may either decrease opioid inhibition of LH secretion or decrease pituitary LH responsiveness to endogenous GnRH released by NAL.

Animals↗
PubMed1986

Influence of stage of the estrous cycle on endogenous opioid modulation of luteinizing hormone, prolactin, and cortisol secretion in the gilt.

Fourteen gilts that had displayed one or more estrous cycles of 18-22 days (onset of estrus = Day 0) and four ovariectomized (OVX) gilts were treated with naloxone (NAL), an opiate antagonist, at 1 mg/kg body weight in saline i.v. Intact gilts were treated during either the luteal phase (L, Day 10-11; n = 7), early follicular phase (EF, Day 15-17; n = 3), or late follicular phase (LF, Day 18-19; n = 4) of the estrous cycle. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. Serum luteinizing hormone (LH) concentrations for L gilts averaged 0.65 +/- 0.04 ng/ml during the pretreatment period and increased to an average of 1.3 +/- 0.1 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum prolactin (PRL) concentrations for L gilts averaged 4.8 +/- 0.2 ng/ml during the pretreatment period and increased to an average of 6.3 +/- 0.3 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum PRL concentrations averaged 8.6 +/- 0.7 ng/ml and 7.6 +/- 0.6 ng/ml in EF and LF gilts, respectively, prior to NAL treatment, and decreased (p less than 0.05) to an average of 4.1 +/- 0.2 ng/ml and 5.6 +/- 0.4 ng/ml in EF and LF gilts, respectively, during the fourth h after NAL. Naloxone treatment failed to alter serum LH concentrations in EF, LF, or OVX gilts and PRL concentrations in OVX gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effect of naloxone on serum luteinizing hormone, cortisol and prolactin concentrations in anestrous beef cows.

Two experiments were conducted with the opioid antagonist naloxone to determine the effect of opioid receptor blockade on hormone secretion in postpartum beef cows. In Exp. 1, nine anestrous postpartum beef cows were used to measure the effect of naloxone on serum luteinizing hormone (LH), cortisol and prolactin concentrations. Cows received either saline (n = 4) or 200 mg naloxone in saline (n = 5) iv. Blood samples were collected at 15-min intervals for 2 h before and after naloxone administration. Serum LH concentrations increased (P less than .01) in naloxone-treated cows from 1.8 +/- .04 ng/ml before treatment to 3.9 +/- .7 ng/ml and 4.2 +/- .5 ng/ml at 15 and 30 min, respectively, after naloxone administration. In contrast, LH remained unchanged in saline-treated cows (1.6 +/- .3 ng/ml). Serum cortisol and prolactin concentrations were not different between groups. In Exp. 2, 12 anestrous postpartum beef cows were used to examine the influence of days postpartum on the serum LH response to naloxone. Four cows each at 14 +/- 1.2, 28 +/- .3 and 42 +/- 1.5 d postpartum received 200 mg of naloxone in saline iv. Blood samples were taken as in the previous experiment. A second dose of naloxone was administered 2 h after the first, and blood samples were collected for a further 2 h. Serum LH concentrations increased (P less than .01) only in cows at 42 d postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)

Anestrus↗
PubMed1986

Influence of calf removal on the serum luteinizing hormone response to naloxone in the postpartum beef cow.

Twelve anestrous, postpartum beef cows were used to determine the effect of calf removal on the effect of naloxone on serum luteinizing hormone (LH) concentrations. On d 1, six cows were injected iv with saline and six with 200 mg naloxone dissolved in saline. Blood samples were taken at 15-min intervals for 2 h before and 2 h after naloxone or saline administration. At the beginning of blood sampling, calves were removed from three cows in each treatment. At 48 h after calf removal (d 3), all cows were injected iv with 200 mg naloxone and blood samples were collected as on d 1. On d 1, naloxone treatment increased (P less than .01) serum LH concentrations from 1.2 +/- .3 ng/ml at time 0 to 4.3 +/- .6 ng/ml and 4.7 +/- .8 ng/ml at 15 and 30 min, respectively. Injection of saline had no effect on serum LH concentrations. Forty-eight-hour calf removal increased (P less than .01) serum LH concentrations in five of six cows (1.7 +/- .8 vs 4.4 +/- 1.2 ng/ml). Naloxone treatment failed to increase serum LH concentrations in these cows. Injection of naloxone increased (P less than .01) serum LH concentrations in the one cow that did not exhibit an LH increase after calf removal and in six cows whose calves were not removed (1.4 +/- .2 vs 4.4 +/- .5 ng/ml). The present study provides additional evidence that endogenous opioids regulate LH in the postpartum beef cow. We hypothesize that suckling stimulates an opioid inhibition of LH secretion and removal of the suckling stimulus removes the opioid inhibitory tone.

Animals↗
PubMed1986

Opioid inhibition of luteinizing hormone secretion during the postpartum period in suckled beef cows.

Recent studies have shown that naloxone (N), an opioid antagonist, increases concentrations of luteinizing hormone (LH) in the postpartum anestrous beef cow. However, the LH response to N was influenced by the postpartum interval. For example, a significant LH response to 200 mg of N occurred on d 42 but not on d 14 or 28 postpartum. The present study was conducted to determine the effect of different doses of N on LH secretion during the postpartum period of beef cows. Twelve cows were given 200, 400 or 800 mg of N on d 14, 28 and 42 postpartum in a Latin square design with repeat measures within cells. On d 14, serum concentrations of LH increased (P less than .01) from .5 +/- .1 ng/ml (mean +/- SE) before N to a peak of 2.0 +/- .5 and 1.4 +/- .5 ng/ml for cows given 400 and 800 mg of N, respectively. In contrast, 200 mg of N had no effect on serum concentrations of LH. On d 28 and 42 all three doses of N elevated (P less than .01) serum concentrations of LH. Therefore, a larger dose of N was required to increase serum concentrations of LH on d 14 postpartum compared with d 28 and 42. Based on these data we suggest that endogenous opioids participate in the regulation of LH secretion in the early postpartum period. The differential response to naloxone may be due to changes in endogenous opioid inhibition of LH secretion during the postpartum period.

Animals↗
PubMed1984

Luteinizing hormone receptors and progesterone content in porcine corpora lutea after prostaglandin F2 alpha.

The effect of prostaglandin F2 alpha (PGF2 alpha) on luteinizing hormone (LH) receptors, weight and progesterone content of corpora lutea (CL), and serum progesterone concentrations was studied in gilts. Fifteen gilts were hysterectomized between Days 9 to 11 of the estrous cycle. Twelve gilts were injected i.m. with 10 mg of PGF2 alpha and 3 with saline on Day 20. Ovaries were surgically removed from each of 3 gilts at 4, 8, 12 and 24 h following PGF2 alpha treatment and from the 3 control gilts 12 h following saline injection. Jugular blood samples for progesterone analysis were collected from all gilts at 0, 2 and 4 h following treatment and at 8, 12 and 24 h for gilts from which ovaries were removed at 8, 12 and 24 h, respectively. Mean serum progesterone and CL progesterone concentrations decreased within 4 h after PGF2 alpha treatment (P less than 0.05) and remained low through 24 h after treatment. The number of unoccupied LH receptors decreased by 4 h (P less than 0.05) and this trend continued through 24 h. There were no differences in luteal weight or affinity of unoccupied LH receptors of luteal tissue at 4, 8 12 and 24 h after PGF2 alpha when compared to luteal tissue from controls. These data indicate that during PGF2 alpha-induced luteolysis in the pig, luteal progesterone, serum progesterone concentrations and the number of LH receptors decrease simultaneously.

Animals↗
PubMed1984

Comparison of physiological indicators of chronic stress in confined and nonconfined gilts.

Two experiments were conducted to determine if confinement-induced delayed puberty in gilts was due to chronic physiological stress imposed by confinement housing. In both experiments, crossbred gilts, raised in total confinement, were moved to an outside dirt lot (nonconfined) or to a single pen in a confinement finishing unit (confined) at 100 to 110 d of age. Beginning at 150 d of age, estrus was checked daily with a boar to determine age at first estrus. Gilts were necropsied at 270 d of age. In Exp. I, 19 confined and 19 nonconfined gilts were cannulated by jugular puncture at 185 d of age. The day after cannulation, blood samples were collected for 4 h, 200 IU porcine adrenocorticoptropic hormone (ACTH) was injected via the cannulae and blood samples were collected for an additional 8 h. Serum cortisol, progesterone, luteinizing hormone (LH) and prolactin (PRL) concentrations were determined. In Exp. II, both jugular veins of six confined and six nonconfined gilts were cannulated at 204 d of age. The day after cannulation, blood samples were collected for 4 h and cortisol was continuously infused for the last 2 h of the blood collection period. Cortisol metabolic clearance rate (MCR) and secretion rate (SR) were determined. By 270 d of age, 21 of 28 (75%) nonconfined gilts and 11 of 31 (35.5%) confined gilts (P less than .01) in Exp. I and 18 of 25 (72%) nonconfined gilts and 12 of 25 (48%) confined gilts (P less than .06) in Exp. II had exhibited estrus and ovulated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Serum luteinizing hormone in prepuberal gilts after ovariectomy or adrenalectomy.

Serum luteinizing hormone (LH) concentrations after ovariectomy (OVX) and adrenalectomy (ADX) were studied in the prepuberal gilt. In Exp.I, gilts, 170 to 175 d of age and 80 to 85 kg body weight, were OVX (n = 5) or sham-OVX (n = 5). Blood samples were collected via jugular vein cannulae every 30 min for 8 h on d 1, 3, 5, 7 and 21 after surgery. In Exp. II, blood samples were collected via jugular vein cannulae every 30 min for 12 h on d 3, 5, 7 and 14 after surgery from five ADX, five sham-ADX and five nonsurgical control gilts of similar ages and weights as in Exp. I. In Exp. I, basal serum LH concentrations (means +/- SE, ng/ml) over all days were greater (P less than .05) in OVX (2.9 +/- .1) than in sham-OVX (1.1 +/- .2) gilts. Average basal serum LH concentrations were greater (P less than .05) on d 1 for both treatments than all other days sampled. The frequency of LH peaks (means +/- SE/8 h) was also greater (P less than .01) for OVX (3.5 +/- .3) than sham-OVX gilts (1.7 +/- .2). Similarly, the mean concentration of the LH peaks was greater (P less than .01) for OVX (4.1 +/- .2 ng/ml) than sham-OVX gilts (2.1 +/- .2 ng/ml). In Exp. II, mean basal serum LH concentrations, frequency of LH peaks and mean concentration of the LH peaks were similar for all treatments on each day sampled. The frequency of LH peaks (means +/- SE/12 h) was greater (P less than .05) on d 3 (3.4 +/- .3) than on d 5 (2.3 +/- .3) and d 7 (2.1 +/- .4), but similar to d 14 (2.8 +/- .5) in all treatments. In prepuberal gilts, ADX failed to influence serum LH concentration, whereas OVX caused a significant increase in serum LH concentration. We suggest that the ovary is the major steroid-secreting gland having a negative feedback on pituitary gonadotropin production in the prepuberal gilt.

Adrenal Glands↗
PubMed1982

Plasma estradiol, thyroid hormones, and liver lipid content in laying hens fed different isocaloric diets.

Two experiments were conducted with laying hens fed a corn-soy basal diet or diets containing fish meal, distillers dried grains with solubles (DDGS) or torula yeast formulated to be isocaloric and isonitrogenous with the basal diet. One half of the hens were kept at a temperature range of 13-24 degrees and the other half at 24-35 degrees for 49 days in experiment 2. Liver lipid content was significantly lower in hens fed DDGS (experiment 1) and DDGS or fish meal (experiment 2) than in hens fed the corn-soy basal diet, but it was not influenced by environmental temperature. Feeding DDGS or fish meal reduced lipoprotein lipase activity in adipose tissue. High temperature reduced plasma estradiol level but not thyroid hormone levels. Plasma estradiol in the hens fed DDGS or fish meal (experiment 1) and DDGS, fish meal or torula yeast (experiment 2) an plasma thyroxine and triiodothyronine in hens fed the DDGS or fish meal at 24-35 degrees in experiment 2 were significantly lower than that of hens fed the corn-soy basal diet. Significant correlations were observed between liver lipid content and plasma estradiol or thyroxine concentrations. These findings show that plasma estrogen and thyroxine levels were influenced by diet composition and that these hormones have a close relation to induction of fatty livers in laying hens.

Animals↗
PubMed1982

Inhibition of ovulation and LH secretion in the gilt after treatment with ACTH or hydrocortisone.

Treatment with ACTH (100 i.u.) or hydrocortisone acetate (250 mg) twice daily for 12 days to increase cortisol concentrations blocked ovulation in all gilts. The preovulatory surge of LH was also blocked in the treated gilts. Oestrous cycle length and number of days in oestrus were similar for all treatments except that in one of the 2 experiments ACTH suppressed oestrus in 4 of the 5 gilts treated.

Adrenocorticotropic Hormone↗
PubMed1981

Serum luteinizing hormone, testosterone, prolactin and cortisol concentrations after PGF2 alpha in the boar.

The effect of prostaglandin F2 alpha (PGF2 alpha) on serum luteinizing hormone (LH), testosterone (T), prolactin (PRL) and cortisol (CS) was studied in the boar. Indwelling cannulae were placed nonsurgically in the jugular vein of six 8 to 9 month-old boars weighing 130 to 160 kilograms. Twenty-four hr after cannulation, blood samples were collected every 30 min from 0630 to 1830 hours. Immediately after the second blood sample (0700 hr) three boars were injected intramuscularly (IM) with 20 mg PGF2 alpha and three boars were injected IM with saline (C). Serum concentrations of LH, T, PRL and CS were quantitated by radioimmunoassay. Serum LH and T concentrations were similar for the PGF2 alpha and C boars throughout the sampling period. In contrast, PRL and CS increased from basal concentrations (mean +/- SE) of 2.1 +/- .1 ng/ml and 24.0 +/- .9 ng/ml to 11.6 +/- .3 ng/ml and 86.9 +/- 9.8 ng/ml, respectively, within 30 min after PGF2 alpha injections and then decreased to control levels over the next 2.0 to 2.5 hours.

Animals↗