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Biomedical subjects

G B Rampacek

Publications and source records attributed to G B Rampacek.

At least 55 records · Page 3Linked to original sources
PubMed1991

Serum glucose and free fatty acids modulate growth hormone and luteinizing hormone secretion in the pig.

Two experiments were conducted to determine the effect of free fatty acids (FFA) and glucose treatment on growth hormone (GH) and luteinizing hormone secretion in the pig. In Experiment (Exp) 1, 15 prepuberal gilts received an intravenous infusion of FFA (n = 5; 3 ml of 10% Liposyn II/kg), glucose (n = 5; 1 g/kg), or saline (n = 5; 3 ml of 0.9%/kg). Jugular blood samples were collected every 15 min for 2 hr before and 3 hr after intravenous infusion of saline, FFA, and glucose. Synthetic [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (1 microgram/kg) and gonadotropin-releasing hormone (0.2 micrograms/kg) were administered 30 min after infusion (Time 0 = infusion). In Exp 2, eight prepuberal gilts received either FFA (n = 4) or saline (n = 4) as described in Exp 1, except that treatments were given every hour ove a 10-hr period. Blood samples were collected every 15 min from 1 hr before to 10 hr after the start of FFA or saline infusion. In Exp 1, the peak GH response to growth hormone-releasing factor was delayed by 45 min (P less than 0.01) by glucose treatment and suppressed (P less than 0.01) by FFA treatment. The luteinizing hormone response to gonadotroph-releasing hormone was suppressed (P less than 0.03) by glucose and enhanced (P less than 0.03) by FFA. In Exp 2, the number of GH pulses was increased (P less than 0.05) by FFA infusion and GH concentrations were positively correlated (r = 0.58, P less than 0.0003) with FFA concentrations, while luteinizing hormone pulse amplitude was greater (P less than 0.01) in FFA gilts than in saline gilts. These results indicate that FFA are more effective modulators of GH secretion than acute hyperglycemia, while metabolic status can alter pituitary responsiveness to gonadotropin-releasing hormone.

Animals↗
PubMed1990

Follicle growth in hypophysial stalk-transected pigs given pulsatile GnRH and pregnant mare serum gonadotropin.

In experiment 1, nine prepuberal crossbred gilts 145 +/- 2 days of age and 90.3 +/- 1.6 kg body weight (BW) were hypophysial stalk-transected (HST) or sham-HST. Starting at 0800 on Day 1 (35 +/- 2 days after surgery), three sham-HST and two HST gilts received 3.5% sodium citrate vehicle (V) while two HST gilts and two sham-HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 9 days via a jugular vein cannula. At 0800 on day 7, all gilts received 1,000 IU of pregnant mare serum gonadotropin (PMSG) im. Blood was sampled every 15 min from 0800 to 0845 on Days 1 through 6. On Day 10, ovarian morphology and ovarian and follicular fluid weights were recorded. In experiment 2, eight prepuberal crossbred gilts, 146 +/- 6 days of age and 79.5 +/- 1.5 kg BW, were HST or sham-HST. Starting at 0800 on Day 1 (7 +/- 4 days after surgery), two sham-HST and three HST gilts received V, while three HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 8 days. At 1200 on Day 5, all gilts, including three unoperated controls (UC), received 1,000 IU of PMSG im. Blood was sampled from all but UC gilts every 15 min from 0800 to 0845 on Days 1 through 5. Ovarian data were obtained on Day 9. The HST + V gilts failed to respond to PMSG, whereas growth of ovulatory follicles was stimulated in the other groups in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Opioid modulation of LH secretion by pig pituitary cells in vitro.

The effects of naloxone and beta-endorphin on LH secretion by pig pituitary cells were studied in primary cultures. On Day 4 of culture, cells (10(5) seeded/well) were challenged with 10(-9), 10(-8) or 10(-7) M gonadotrophin-releasing hormone (GnRH), 10(-10), 10(-9), 10(-8) or 10(-7) M-beta-endorphin or 10(-6) M-naloxone individually or in combinations. Secreted LH was measured at 4 h and 24 h after treatment and cellular content of LH was measured after 24 h. Basal LH secretion (control) was 23.5 +/- 7.6 and 36.9 +/- 10.3 ng/well at 4 h and 24 h, respectively. Relative to control at 4 h, 10(-9), 10(-8) or 10(-7) M-GnRH stimulated (P less than 0.05) LH secretion 140%, 210% and 250%, respectively. At 24 h, LH secretion was increased (P less than 0.05) by GnRH compared to control, but the dose-response to GnRH was absent. Naloxone increased (P less than 0.01) LH secretion 166 +/- 13% at 4 h and 141 +/- 13% (P less than 0.06) at 24 h. Secretion of LH after simultaneous addition of 10(-8) M-GnRH plus naloxone was greater (P less than 0.01) than after GnRH alone at 4 h but not at 24 h. beta-Endorphin at 10(-10), 10(-9), 10(-8) or 10(-7) M failed to alter basal LH secretion at 4 h but decreased secretion at 24 h, while cellular LH content was similar to control at 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Gonadotropin and prolactin secretion following intraventricular administration of morphine in gilts.

The effects of central nervous system administration of morphine on secretion of luteinizing hormone (LH), follicle-stimulating hormone, and prolactin were investigated in ovariectomized gilts stereotaxically implanted with lateral ventricular cannulas. In Experiment 1, mean serum LH and follicle-stimulating hormone concentrations and serum LH pulse frequency were unaffected by artificial cerebrospinal fluid administration (P greater than 0.1), but decreased (P less than 0.01) in 8 of 11 gilts when 500 micrograms of morphine were given 3 hr later. Serum LH pulse amplitude was unaffected (P greater than 0.1) by cerebrospinal fluid or morphine injection. In Experiment 2, luteinizing hormone concentrations decreased (P less than 0.0001) and prolactin concentrations increased (P less than 0.0001), but follicle-stimulating hormone concentrations did not change (P greater than 0.1) after 500 micrograms of morphine. Gonadotropin responses to 10 micrograms of gonadotropin-releasing hormone, given 2 hr after intraventricular injection, were similar (P greater than 0.1) for morphine- and cerebrospinal fluid-treated gilts. These results indicate that morphine inhibits LH secretion at the level of the central nervous system, and are consistent with the concept that endogenous opioid peptides participate in the regulation of gonadotropin and prolactin release in pigs.

Analysis of Variance↗
PubMed1989

Luteinizing hormone secretion following intracerebroventricular administration of morphine in the prepuberal gilt.

Antagonism of endogenous opioids with naloxone stimulates luteinizing hormone (LH) release in mature but not prepuberal gilts. The present report demonstrates that the opiate agonist morphine (500 micrograms), administered intracerebroventricularly (ICV), reduced LH secretion in both ovariectomized mature and prepuberal gilts. We suggest that opioid receptors are functionally coupled to the GnRH secretory system in prepuberal gilts even though endogenous opioid peptide modulation of LH secretion was not demonstrable in our previous studies.

Animals↗
PubMed1989

Localization of proopiomelanocortin (POMC) immunoreactive neurons in the forebrain of the pig.

The distribution of proopiomelanocortin (POMC)-immunoreactive neurons was examined in the forebrains of nine sexually mature female pigs by indirect biotin-avidin horseradish peroxidase immunocytochemistry. Primary antiserum against ovine beta-endorphin (Bioflex #BF-EP-3-1) yielded positive staining of neuronal perikarya and processes. Adjacent control sections treated either with primary antiserum preabsorbed with beta-endorphin or substituted with normal rabbit serum lacked specific staining. POMC-immunoreactive cells were located in the anterior and intermediate lobe of the pituitary gland. POMC-immunoreactive perikarya were located in the arcuate nucleus and periarcuate area. The pituitary stalk/median eminence contained sparsely distributed POMC-immunoreactive fibers, which were confined to the zona interna. POMC-immunoreactive fibers were located in the arcuate nucleus and extended rostrally from the arcuate nucleus into the telencephalon coursing adjacent to the wall of the third ventricle as well as through the anterior hypothalamus, suprachiasmatic, supraoptic nuclei and preoptic areas to the nucleus accumbens, diagonal band of Broca, olfactory tubercle, bed nucleus of the stria terminalis and the ventro-lateral aspect of the septum. Caudal projections extended along the wall of the third ventricle to the level of the mammillary bodies and also coursed dorsally, passing through the periventricular, paraventricular, and dorsal medial nuclei of the hypothalamus to the midline thalamic nuclei and habenular nucleus. Lateral projections extended from the arcuate nucleus along the dorsal aspect of the optic tract and terminated in the amygdaloid complex. The distribution of POMC-immunoreactive perikarya and fibers is similar to that of the luteinizing hormone-releasing hormone (LHRH) fiber network. Therefore the opportunities exist, anatomically, for interactions between the POMC and the LHRH systems.

Animals↗
PubMed1989

Negative feedback as an obligatory antecedent to the estradiol-induced luteinizing hormone surge in ovariectomized pigs.

In ovariectomized pigs, estradiol treatment induces a preovulatory-like luteinizing hormone (LH) surge, but only after serum LH concentrations are suppressed for 48 h. This inhibition of LH release is attributable in large part to inhibition of gonadotropin-releasing hormone (GnRH) release. The present report examines the dependency of the estradiol-induced LH surge on this preceding phase of negative feedback. Ten ovariectomized gilts were given an i.m. injection of estradiol benzoate (10 micrograms/kg BW). Beginning at the time of estradiol treatment, 5 of these gilts received 1-microgram GnRH pulses i.v. every 45 min for 48 h, i.e. during the period of negative feedback. The remaining 5 control gilts received comparable infusions of vehicle. Estradiol induced the characteristic biphasic LH response in control gilts. On the other hand, the inhibitory LH response to estradiol was prevented and the ensuing LH surge was blocked in 4 of the 5 gilts given GnRH pulses during the negative feedback phase. These results indicate that suppressing release of GnRH and/or LH is an important antecedent to full expression of the LH surge in ovariectomized pigs. Assimilation of this observation with the existing literature provides novel insights into the neuroendocrine control of LH secretion in castrated and ovary-intact gilts.

Animals↗
PubMed1989

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

To determine the sites of action whereby estradiol (E2) induces the preovulatory luteinizing hormone (LH) surge in pigs, hypophysial-stalk-transected (HST) ovariectomized (OVX) gilts (mean +/- SE: 118 +/- 12 kg) received intramuscular injections of E2 benzoate (10 micrograms E2B/kg body weight) on day 0, plus intravenous pulses of 1 microgram gonadotropin-releasing hormone (GnRH) every 45 min either from days -5 to 4, days -5 to 0 or days -5 to 0 then days 2 to 4. A fourth and fifth group received steroid vehicle on day 0 and pulses of GnRH on either days -5 to 4 or days -5 to 0 then days 2 to 4. In stalk-intact OVX gilts, E2B inhibited LH release for 48 h, then induced an LH surge that peaked 60-84 h after steroid treatment. In HST OVX gilts, serum LH increased from undetectable concentrations (less than 0.17 ng/ml) to 0.42 +/- 0.03 ng/ml after 5 days of pulsatile GnRH replacement. In the presence of pulsatile GnRH stimulation, serum LH concentrations were inhibited for 12 h after E2B but then returned to values that were similar to those for HST gilts given GnRH in the absence of steroid treatment. Discontinuing GnRH pulses at the time of E2B injection caused serum LH concentrations to drop to 0.18 ng/ml or less for the remaining 96 h. When GnRH pulses were interrupted for 48 h, beginning immediately after injecting E2B or vehicle to mimic the secretory hiatus of LH and presumably GnRH observed in stalk-intact pigs prior to the surge, resumption of GnRH pulses caused serum LH concentrations to increase progressively over 3 h in E2B-treated gilts but to peak abruptly in controls given vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Influence of the ovary and suckling on luteinizing hormone response to naloxone in postpartum beef cows.

The influence of the suckling stimulus and ovarian secretions on LH response to naloxone was studied in 16 postpartum anestrous beef cows that were assigned randomly to one of four groups (n = 4/group): intact suckled (IS), intact nonsuckled (IN), ovariectomized suckled (OS) or ovariectomized nonsuckled (ON). Ovariectomy (OS + ON) and calf removal (IN + ON) were performed on d 2, 3 or 4 after parturition. Jugular venous blood was collected at 15-min intervals for 4 h before and 4 h after administration of naloxone (1 mg/kg BW, i.v.) on d 14 and d 28 after parturition. Gonadotropin-releasing hormone (5 micrograms, i.v.) was given 3 h after naloxone. Both IN and OS increased (P less than .05) mean pretreatment LH above IS values (mean +/- SE, ng/ml; IS 1.6 +/- .1 vs IN 2.5 +/- .3 and OS 2.7 +/- .4; P less than .01), whereas ON increased (P less than .01) LH (3.7 +/- .3 ng/ml) even further. Mean LH increased (P less than .05) after naloxone administration in all treatment groups. However, magnitude of this response was variable and dependent on ovarian status. Amplitude of the naloxone-induced LH response was greater (P less than .05) for ovariectomized (5.9 +/- 1.1 ng/ml) than for intact groups (2.7 +/- .5 ng/ml). Gonadotropin-releasing hormone increased mean LH concentrations in all groups. We suggest that ovarian secretions and the suckling stimulus contribute to endogenous opioid inhibition of LH during the postpartum interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

Localization of luteinizing hormone-releasing hormone in the forebrain of the pig.

The distribution of luteinizing hormone-releasing hormone (LHRH)-immunostained perikarya and processes was examined in the forebrains of six sexually mature female pigs by use of indirect biotin-avidin horseradish peroxidase immunocytochemistry. Two primary antisera (Drs. Y.F. Chen and V.D. Ramirez CRR11B73 and Miles-Yeda UZ-4) yielded positive staining. Adjacent sections treated either primary antiserum preabsorbed with LHRH or with normal rabbit serum substituted for primary antiserum lacked positive staining. The greatest proportion of LHRH-immunostained perikarya were found in the medial preoptic area adjacent to the organum vasculosum of the lamina terminalis. The LHRH-immunostained perikarya were also scattered rostrally in the diagonal band of Broca, and within the lateral hypothalamic area, paraventricular nucleus, periventricular zone, suprachiasmatic nucleus, and medial basal hypothalamus. LHRH-immunostained processes, which extended from the medial preoptic area, coursed either along the ventral surface to the median eminence or medially and ventrally along the third ventricular wall ventrally to the median eminence and caudally to the level of the mammillary bodies. Extrahypothalamic processes were located adjacent to the lateral ventricular floor and the third ventricle from the lateral septal area (stria terminalis) to the level of the habenular nucleus. LHRH-immunostained neurons were unipolar, bipolar, and multipolar. Close associations between individual LHRH-immunostained neurons were observed.

Animals↗
PubMed1988

Serum concentrations of prolactin, oestrogen and LH during the perioestrous period in prepubertal gilts induced to ovulate and mature gilts.

The temporal relationships of serum prolactin, oestrogen and LH concentrations during the perioestrous period were compared in prepubertal gilts induced to ovulate by PMSG and hCG and in mature gilts. In Exp. 1, 2 sustained prolactin surges, beginning 4 days and 1 day before the preovulatory LH surge, occurred in all mature gilts. A single preovulatory prolactin surge occurred in 3 prepubertal gilts, starting just before the preovulatory LH surge, but 4 prepubertal gilts had neither a prolactin nor an LH surge. A status (prepubertal or mature) versus time interaction (P less than 0.01) was detected for serum prolactin concentrations. A preovulatory oestrogen surge occurred in all gilts but was of lesser magnitude (P less than 0.01) and duration (P less than 0.05) in the prepubertal gilts without prolactin and LH surges compared to mature gilts and of lesser magnitude (P less than 0.01) compared to prepubertal gilts with prolactin and LH surges. The relative timing of the oestrogen surge in prepubertal gilts corresponded with that of mature gilts when adjusted to the LH surge (if present) but was delayed (P less than 0.01) in all prepubertal gilts if standardized to the hCG injection. In Exp. 2, mature gilts were examined to determine whether 2 perioestrous prolactin surges were characteristic of all cycling gilts. Of 9 gilts, 8 exhibited an initial prolactin surge 4-5 days before oestrus and 5/9 gilts exhibited a periovulatory prolactin surge. The presence of 2 perioestrous serum prolactin surges was not a requirement for subsequent pregnancy maintenance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of dietary energy source and level on serum growth hormone, insulin-like growth factor 1, growth and body composition in beef heifers.

Effects of fiber vs starch energy supplements on endogenous growth hormone (GH), insulin-like growth factor (IGF-1) and animal performance from weaning to breeding age were evaluated in 18, 9-mo-old beef heifers. Heifers had ad libitum access to wheat silage plus an average daily supplement intake of 1) 4.08 kg corn-soybean meal (SBM) (high energy-starch, HS), 2) 4.54 kg soyhulls (SH)-SBM (high energy-fiber, HF) or 3) 1.36 kg SH-SBM (low energy-fiber, LE). Serum samples were collected via jugular puncture every 10 d and were analyzed for IGF-1 by RIA. On d 45 and d 176, four heifers per treatment were fasted 18 h and serial blood samples collected via jugular cannulas every 15 min for 6.5 h. Arginine (.5 g/kg BW) was administered intravenously (ARG) to induce release of GH, and four additional samples of blood were collected. Samples were analyzed by RIA for GH. Mean fasted GH (6.4 +/- .4, 8.3 +/- .4 and 13.8 +/- .4 ng/ml for HS, HF and LE, respectively) varied with energy source and level (P less than .01). Mean GH following ARG was higher (P less than .01) in heifers receiving LE (46.2 +/- 4.7) than in those receiving HS and HF (23.5 +/- 4.4 and 24.1 +/- 4.6 ng/ml). Basal GH concentration and peak amplitude were higher (P less than .05) in LE than in HS and HF treatments. Diet did not influence number or frequency of GH peaks.(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↗