Biomedical subjects

H A Tucker

Publications and source records attributed to H A Tucker.

At least 19 recordsLinked to original sources

PubMed1998

Stimulation of dopamine D1 receptors increases activity of periventricular somatostatin neurons and suppress concentrations of growth hormone.

The selective dopamine D1 receptor agonist, SKF38393, stimulates release of somatostatin (SS) from perifused bovine hypothalamic slices. Therefore, we hypothesized that SKF38393 activates SS neurons, which, via release of SS, would suppress concentrations of growth hormone (GH) in serum in calves. Our objectives were to determine whether SKF38393: (1) increases the percent of immunoreactive c-Fos protein and Fos-related antigens (Fos/FRA) detected in somatostatin neurons in periventricular (PeVN) and arcuate (ARC) hypothalamic nuclei; (2) reduces concentrations of GH in serum; (3) suppresses growth hormone-releasing hormone (GHRH)-induced release of GH. Meal-fed steers were used to perform these objectives because a synchronous pulse of GH occurs 1-2 hr before feeding in steers allowed access to feed for 2 hr each day. In Experiment 1, two groups of four Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW). Steers were injected i.v. with a lethal dose of sodium pentobarbital 100 min later and their brains were fixed with 4% paraformaldehyde. Dual-label immunohistochemistry was performed on 40 microns free-floating sections using antiserum to SS and to Fos/FRA on sections containing PeVN and ARC nuclei. More SS neurons were detected in the PeVN than in the ARC. The percent of SS neurons with immunoreactive Fos/FRA present was 2.9-fold higher in SKF38393-treated compared with vehicle-injected steers in the PeVN, but was unchanged in the ARC. In Experiment 2, eight Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW) 140 min before meal-feeding. In contrast to controls, concentrations of GH in serum of SKF38393-treated steers did not increase during 140 min before meal-feeding. In Experiment 3, eight Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW), then 100 min later, each steer was injected i.v. with [Leu27,Hse45] bGHRH1-45 lactone (0.2 micrograms/kg BW). Bovine GHRH stimulated release GH into serum in both groups, but concentrations of GH were lower in SKF38393-treated steers. These results show that stimulation of D1 receptors selectively increases activity of SS neurons in the PeVN, and this increased activity is associated with suppressed basal- and GHRH-induced release of GH in serum of meal-fed steers.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1997

Regulation of growth hormone-releasing hormone and somatostatin from perifused, bovine hypothalamic slices. I. Alpha 2-adrenergic receptor regulation.

An in vitro perifusion system was developed for bovine hypothalamic tissue to examine the role of alpha 2-adrenergic receptors in the regulation of growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) release. Up to three sagittal slices (600 microns) of hypothalamus, immediately parallel to the midline, were cut in an oxygenated balanced salt solution at 4 degrees C, placed in 5 cc syringes, and perifused at 37 degrees C with oxygenated minimum essential medium-alpha at a flow rate of 0.15 ml/min. Three experiments were conducted, and medium effluent was collected every 20 min before (two samples), during (one or three samples), and after (six samples) treatment. Areas under GHRH and SRIF response curves (AUC), adjusted by covariance for pretreatment values, were calculated from samples collected during the treatment/post-treatment period. Location from which slices were cut, relative to the sagittal midline, had no effect on basal release of GHRH and SRIF, but variation in basal release of GHRH and SRIF differed among animals. Medium containing 60 mM KCI increased AUC for GHRH 39% and 161% for SRIF when compared with perifusion of medium alone, thereby verifying that tissue remained viable for at least 14 hr. Activation of alpha 2-adrenergic receptor with 10(-6) and 10(-4) M clonidine increased AUC for GHRH from 54.8 (control) to 79.1 and 108.7 +/- 2.5 ng.ml-1 min for 10(-6) M and 10(-4) M clonidine, respectively. Guanabenz, another alpha 2-adrenergic receptor agonist, at 10(-8), 10(-6), and 10(-4) M also increased GHRH release from 45.5 (control) to 52.8, 66.2, and 86.7 +/- 1.6 ng.ml-1 min, respectively. Clonidine and guanabenz did not affect release of SRIF. An alpha 2-adrenergic receptor antagonist, idazoxan, blocked clonidine-induced release of GHRH without affecting release of SRIF. We concluded that alpha 2-adrenergic receptor stimulation of in vivo growth hormone secretion in cattle is mediated via an increase in release of GHRH and not a change in release of SRIF.

Adrenergic alpha-Agonists↗

PubMed1997

Regulation of growth hormone-releasing hormone and somatostatin from perifused, bovine hypothalamic slices. II. Dopamine receptor regulation.

An in vitro perifusion system for bovine hypothalamic tissue was utilized to examine the role of D1 and D2 dopamine receptors in the regulation of somatostatin (SRIF) and growth hormone-releasing hormone (GHRH) release. Up to three sagittal slices (600 microns) of bovine hypothalamus, immediately parallel to the midline, were cut in an oxygenated balanced salt solution at 4 degrees C, placed in 5 cc syringes, and perifused at 37 degrees C with oxygenated minimum essential medium-alpha at a flow rate of 0.15 ml/min. Five experiments were conducted, and medium effluent was collected every 20 min before (two samples), during (one or three samples), and after (six samples) treatment. Areas under SRIF and GHRH response curves (AUC), adjusted by covariance for pretreatment values, were calculated from samples collected during the treatment/post-treatment period. Activation of D1 receptor with 10(-8) M and 10(-6) M SKF 38393 increased AUC for SRIF from 5.6 (control) to 420 and 500 +/- 57.8 ng.ml-1 min, but 10(-10) M SKF 38393 was ineffective. Relative to controls, release of GHRH was decreased 50% in the 10(-6) M SKF 38393 group. Blockade of D1 receptors with SCH 23390 had no effect on basal release of either SRIF or GHRH, but prevented SKF 38393-induced release of SRIF and SKF 38393-induced suppression of GHRH. In contrast, quinelorane, a D2 receptor agonist, and haloperidol, which blocks D2 receptors, did not affect release of SRIF or GHRH. We concluded that activation of D1 dopamine receptors, but not D2 dopamine receptors, stimulates release of SRIF and inhibits release of GHRH from the bovine hypothalamus.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1997

Regulation of growth hormone-releasing hormone and somatostatin from perifused, bovine hypothalamic slices. III. Reciprocal feedback between growth hormone-releasing hormone and somatostatin.

An in vitro perifusion system for bovine hypothalamic tissue was used to determine if growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) modulate each other's release, and whether SRIF mediates D1-agonist-induced suppression of GHRH in cattle. Up to three sagittal slices (600 microns) of bovine hypothalamus, immediately parallel++ to the midline, were cut in an oxygenated balanced salt solution at 4 degrees C, placed in 5 cc syringe barrels, and perifused at 37 degrees C with oxygenated minimum essential medium-alpha at a flow rate of 0.15 ml/min. Three experiments were conducted, and medium effluent was collected every 20 min before (two samples), during (one or three samples), and after (six samples) treatment. Areas under GHRH and SRIF response curves (AUC), adjusted by covariance for pretreatment values, were calculated from samples collected during the treatment/post-treatment period. Perifusion of SRIF at 10(-6) M and 10(-4) M decreased AUC for GHRH from 86.3 (control) to 65.4 and 59.5 +/- 6.3 ng.ml-1 min, but 10(-8) M SRIF was ineffective. Relative to controls, 10(-8).10(-6), and 10(-4) M GHRH increased release of SRIF 190, 675, and 1,135%, respectively. Activation of D1 receptors with 10(-6) M SKF 38393 increased AUC for SRIF from 12.5 ng.ml-1 min (control) to 484.9 ng.ml-1 min and decreased AUC for GHRH from 36.4 ng.ml-1 min (control) to 18.2 ng.ml-1 min. Blockade of SRIF action with a SRIF antagonist, cyclo-[7-aminoheptanoyl-phe-D-trp-lys-thr(bzl)], increased release of GHRH 1.9-fold. In addition, the SRIF antagonist blocked SKF 38393-induced suppression of GHRH. We concluded that GHRH and SRIF interact within the bovine hypothalamus/pituitary stalk to modulate the release of the other. Moreover, SRIF mediates the inhibitory effects of activation of D1 receptors on release of GHRH in cattle.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1997

Effects of diet and bovine somatotropin on heifer growth and mammary development.

Forty Holstein heifers [body weight (BW) = 126 kg] were blocked by BW into groups of 4, and, within each block, heifers were randomly assigned to one of four treatments. Twenty heifers had ad libitum access to a diet formulated to produce a BW gain of 0.8 kg/d (control diet), and 20 heifers had ad libitum access to a diet formulated to produce a BW gain of 1.2 kg/d. (high diet). Half of the heifers fed each diet were injected daily with bovine somatotropin (bST; 25 micrograms/ kg of BW). The high diet increased daily BW gain as well as body condition score. Injection of bST also increased daily BW gain, but did not affect body condition score. The high diet reduced age at puberty by 58 d, but did not affect BW, withers height at puberty, or pelvic area at slaughter. Injection of bST had no effect on age at puberty, but increased BW, withers height at puberty, and pelvic area at slaughter. The high diet did not affect mammary parenchymal DNA, RNA, or the ratio of RNA to DNA. The injection of bST increased mammary parenchymal DNA, RNA, and the ratio of RNA to DNA. The high diet was more cost effective for rearing dairy heifers from 120 d of age to potential breeding size (> or = 363 kg of BW and postpubertal) than was the control diet. In conclusion, the high protein, high energy diet increased growth rate without detrimental effects on mammary development. Injection of bST increased BW, skeletal size, and mammary development.

Animals↗

PubMed1996

Regulation of glucose transporter gene expression in mammary gland, muscle, and fat of lactating cows by administration of bovine growth hormone and bovine growth hormone-releasing factor.

Primiparous cows received 29 mg of bovine growth hormone (bGH)/d, or 12 mg of bovine growth hormone-releasing factor (bGHRF)/d by continuous i.v. infusion, or no treatment (controls) from 118 to 181 d postpartum. Compared with controls, bGHRF and bGH did not influence the amount of erythrocyte-type glucose transporter (GLUT1) protein in the mammary gland; however, GLUT1 mRNA was increased (P < .01) by bGHRF, but not by bGH. The insulin-responsive glucose transporter (GLUT4) mRNA in skeletal muscle was decreased by 44% (P < .05) as a result of bGH treatment, but there was no significant effect of bGHRF. The GLUT4 mRNA was barely detectable in the omental fat of control cows and became undetectable in bGH-and bGHRF-treated cows. The results of the present study indicate that bGH and bGHRF may increase glucose availability to the mammary gland by regulating glucose transporter expression in skeletal muscle and omental fat. Our data also indicate that the galactopoietic action of bGHRF may not be mediated solely through GH.

Adipose Tissue↗

PubMed1996

Regulation of the gene expression of glucose transporter in liver and kidney of lactating cows by bovine growth hormone and bovine growth hormone-releasing factor.

Our objective was to study the effects of recombinant bovine growth hormone and bovine growth hormone-releasing factor on gene expression of glucose transporters in the liver and kidney of lactating cows. Primiparous cows received 29 mg/d of bovine growth hormone or 12 mg/d of bovine growth hormone-releasing factor by continuous intravenous infusion or no treatment (control) from 118 to 181 d postpartum. Growth hormone or growth hormone-releasing factor did not influence the mRNA abundance of the liver-type glucose transporter in the liver or kidney. Similarly, neither growth hormone-releasing factor nor growth hormone altered the mRNA abundance of the erythrocyte-type or the intestinal-type glucose transporter in the kidney, but large individual differences were observed in the mRNA abundance of the intestinal-type glucose transporter in liver.

Animals↗

PubMed1996

5-hydroxytryptaminergic receptor-mediated regulation of growth hormone secretion in Holstein steers occurs via alpha 2-adrenergic-dependent and -independent mechanisms.

In vitro and in vivo experiments were used to determine the relationship between 5-hydroxytryptaminergic and alpha 2-adrenergic receptors in regulation of growth hormone secretion in cattle. Activation of 5-hydroxytryptaminergic receptors (10(-8), 10(-6), 10(-4) M quipazine) or alpha 2-adrenergic receptors (10(-8), 10(-6), 10(-4) M clonidine) had no effect on secretion of growth hormone from perifused anterior pituitary cells. In vivo, quipazine (0.2 mg/kg body wt, i.v.) and clonidine (8 micrograms/kg body wt, i.v.), when injected separately, each maximized secretion of growth hormone in Holstein steers. However, concurrent administration of quipazine and clonidine at these doses additively increased secretion of growth hormone (mean areas under curves = 439, 914, 1425, and 2359 +/- a pooled SEM of 246 ng.ml-1.min for vehicle, clonidine, quipazine, and quipazine plus clonidine treatments, respectively). Blockade of 5-hydroxytryptaminergic receptors with cyproheptadine (0.2 or 1.0 mg/kg body wt, s.c., 0740 hr) decreased basal concentrations of growth hormone but had no effect on the ability of clonidine (8 micrograms/kg body wt, i.v., 0840 hr) to increase secretion of growth hormone (mean areas under curves = 591, 1218, 363, 1087, and 1002 +/- a pooled SEM of 177 ng.ml-1.min for vehicle-vehicle, vehicle-clonidine, 0.2 mg cyproheptadine-vehicle, 0.2 mg cyproheptadine-clonidine and 1.0 mg cyproheptadine-clonidine treatments, respectively). Blockade of alpha 2-adrenergic receptors with either yohimbine (5 mg/kg body wt, s.c., 0740 hr) or idazoxan (20 mg/kg body wt, s.c., 0740 hr) suppressed both basal and 5-hydroxytryptaminergic receptor-stimulated (0.2 mg quipazine/kg body wt, i.v., 0840 hr) secretion of growth hormone (mean areas under curves = 568, 1252, 410, and 558 +/- a pooled SEM of 108 ng.ml-1.min for vehicle-vehicle, vehicle-quipazine, yohimbine-vehicle, and yohimbine-quipazine treatments, respectively, and means of 553, 1468, 194, and 686 +/- a pooled SEM of 221 ng.ml-1.min for vehicle-vehicle, vehicle-quipazine, idazoxan-vehicle, and idazoxan-quipazine treatments, respectively). We conclude that two mechanisms in the central nervous system mediate 5-hydroxytryptaminergic receptor-stimulated secretion of growth hormone in cattle; one independent and another dependent on alpha 2-adrenergic receptors, possibly via regulation of basal growth hormone secretion. In contrast, alpha 2-adrenergic receptor-induced secretion of growth hormone occurs independently of 5-hydroxytryptaminergic receptors.

Adrenergic alpha-Agonists↗

PubMed1995

Effect of light therapy on salivary melatonin in seasonal affective disorder.

To investigate the role of a light-induced advance in the timing of the melatonin rhythm in seasonal affective disorder, 11 depressed patients underwent 2 weeks of light therapy with full spectrum or cool white light. Evening saliva samples were collected before and after each week of treatment and assayed for melatonin to determine the time of onset of nocturnal secretion. Both treatments reduced depression scores, advanced the timing of the melatonin rhythm, and increased melatonin concentrations. Time of onset of the nocturnal increase in melatonin did not differ between clinical responders and nonresponders, suggesting that a phase advance in the onset of nocturnal melatonin secretion is not sufficient to induce clinical remission in seasonal affective disorder.

Adult↗

PubMed1995

Long-term somatotropic and galactopoietic effects of a (1-30) ethyl amide analog of growth hormone-releasing factor.

Thirty-five lactating Holstein cows (165 +/- 8 DIM) received the following treatments for 96 d: uninfused controls; i.v. infusion of .9, 2.7, or 8.1 mg/d of Ile2, Ser8.28, Ala15, Leu27, Hse30-bovine growth hormone-releasing factor (1-30) ethyl amide; or i.v. infusion of 12 mg/d of recombinant Leu27, Hse45-bovine growth hormone-releasing factor (1-45) lactone. Concentrations of somatotropin in serum and SCM yield of cows infused with 1-30 releasing factor increased quadratically as the dose increased. Responses for somatotropin and SCM yield were quantitatively similar for cows infused with 2.7 and 8.1 mg of 1-30 or 12 mg of 1-45. While concurrently infused with the 1-30 or 1-45 as described, cows retained their ability to release somatotropin following an acute i.v. injection of 10 nmol/100 kg of BW of either growth hormone-releasing factor 1-30 or 1-45. Mean concentrations of IGF-I in serum increased similarly in magnitude for cows infused at all doses of 1-30 or 1-45. The 1-30 releasing factor generally increased IGF-binding protein-3, but had little effect on IGF-binding protein-2. The 1-45 releasing factor did not significantly affect either binding protein. Yield of SCM was correlated with serum concentrations of somatotropin, but not with IGF-I. Concentrations of NEFA in serum were elevated through 36 and 50 d in response to the highest doses of 1-30 and 1-45, respectively. Treatment did not affect DMI, BW, or body condition score.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Comparison of growth hormone-releasing factor and somatotropin: body growth and lactation of primiparous cows.

Growth hormone-releasing factor is the main endogenous stimulator of somatotropin secretion. Our objective was to compare the effects of recombinant growth hormone-releasing factor and recombinant bST on somatotropin secretion, mammary function, and body composition of lactating, primiparous dairy cows. Cows (118 d of lactation) served as uninfused controls or were infused for 63 d with 12 mg/d of releasing factor or with 29 mg/d of bST. These doses elevated somatotropin in serum to concentrations of similar magnitude. The releasing factor and bST each similarly increased milk yield, yield of milk components, weight of most organs, mobilization of adipose tissue, accretion of lean tissue in the carcass, and metabolic activity (RNA) of mammary tissue. Relative to controls, neither releasing factor nor bST significantly affected cell numbers (DNA) in mammary glands or concentrations of plasmin in milk. None of the variables measured provided evidence for galactopoietic effects of releasing factor independent of somatotropin.

Adipose Tissue↗

PubMed1995

Comparison of growth hormone-releasing factor and somatotropin: the somatotropic axis in lactating primiparous cows.

Our objective was to compare the effects of recombinant bovine growth hormone-releasing factor and recombinant bST on the somatotropic cascade in lactating dairy cows. Primiparous cows were killed after 63 d of continuous daily infusion with 12 mg of releasing factor or 29 mg of bST or no infusion (controls). Both hormone infusions similarly increased mean concentration of somatotropin in serum, but pulsatility of somatotropin in serum was greater for cows given releasing factor. Both hormone infusions increased the amounts of IGF-I in serum, IGF-I mRNA in liver, and IGF-binding protein-3 in serum and decreased IGF binding protein-2 in serum, but these effects were less for cows given releasing factor than for those given bST. Both infusions decreased the number of free binding sites for IGF-I in mammary tissue. In liver, treatment did not alter the abundance of mRNA for the somatotropin receptor or the number of free binding sites for somatotropin. Results suggest that endogenous somatotropin is less effective as an IGF-I secretagogue than is exogenous bST infused continuously, yet the releasing factor and bST increased milk yield similarly. We conclude that growth hormone-releasing factor stimulates milk synthesis mostly through the same mechanisms as bST, but that serum IGF-I alone is not a good indicator of the galactopoietic potency of the two hormones.

Animals↗

PubMed1995

Comparison of growth hormone-releasing factor and somatotropin: thyroid status of lactating, primiparous cows.

Effects of recombinant bovine growth hormone-releasing factor and recombinant bST on thyroxine 5'-deiodinase activities of liver and mammary gland were studied for lactating cows. Beginning on d 118 of lactation, 30 primiparous Holsteins received continuous infusions of 12 mg/d of releasing factor or 29 mg/d of bST or served as uninfused controls for 63 d. Blood samples were collected on d 1, 29, and 57, and samples of whole milk were collected at the early afternoon milking on d -5, 30, and 58. Liver and mammary tissue samples were obtained at slaughter on d 63. Infusion of releasing factor and bST decreased serum concentration of triiodothyronine by 10% and the ratio of triiodothyronine to thyroxine in serum by 20%. Concentrations of circulating triiodothyronine reflected a 30% decrease in hepatic 5'-deiodinase activity in response to infusion with releasing factor and bST. In contrast, treatment with releasing factor and bST did not affect 5'-deiodinase activity in the mammary gland and did not alter triiodothyronine concentration in milk. Data suggest that releasing factor and bST increase the hypothyroid status of the lactating cow and maintain an euthyroid condition in the mammary gland, thus enhancing the metabolic priority of the mammary gland.

Animals↗

PubMed1995

Comparison of growth hormone-releasing factor and somatotropin: lipid and glucose metabolism in dairy cows.

Lactating, primiparous Holstein cows were continuously infused for 63 d with either recombinant growth hormone-releasing factor or recombinant bST or were not infused (control). The releasing factor and bST treatments reduced fat synthesis from acetate and lipoprotein lipase activity in omental adipose tissue. Also, both treatments increased hormone-sensitive lipase activity per gram of adipose tissue and reduced fatty acid esterification per milligram of protein in adipose tissue. Protein concentration in adipose tissue with both treatments was greater than that of the control, although the protein concentration was less in adipose tissue from cows treated with the releasing factor than from those treated with bST. In mammary tissue, releasing factor increased fat synthesis from acetate more than did bST treatment, but percentages of fat or short-chain fatty acids in milk were not different between treatments, nor were differences significant between treatments and control for fatty acid esterification or lipoprotein lipase activity in mammary tissue or gluconeogenesis and fatty acid esterification in liver. We conclude that protein concentration was lower in omental adipose tissue of cows treated with releasing factor than that in tissue of cows treated with bST, although both treatments similarly suppressed synthesis of fat from acetate and activity of lipoprotein lipase.

Acetates↗

PubMed1995

5-Hydroxytryptaminergic receptor-stimulated growth hormone secretion occurs independently of changes in peripheral somatostatin concentration.

Effects of activation or blockade of 5-hydroxytryptaminergic receptors on concentrations of growth hormone and somatostatin in serum were studied in Holstein steers (mean +/- SEM: 159 +/- 8 days of age; 160 +/- 9 kg of body wt). A pelleted diet was available ad libitum between 1000 and 1200 hr each day. Blood was sampled from a cannula in a jugular vein. Peak concentration of growth hormone in serum within 1 hr before feeding (12.8 +/- 3.8 ng/ml) was greater than peak concentration within 1 hr after removal of feed (3.3 +/- 1.0 ng/ml). In contrast, concentration of somatostatin in plasma did not change from 1 hr before feeding through 1 hr after removal of feed (47.3 to 43.0 +/- 4.5 pg/ml). Relative to saline-injected controls, activation of 5-hydroxytryptaminergic receptors with quipazine (0.5, 0.1, and 0.2 mg/kg body wt, iv) increased the area under growth hormone response curves 5.5- to 25-fold before and after feeding. In another experiment, injection of 0.1 mg of quipazine/kg body wt at 1300 hr increased the concentration of growth hormone in serum 7.8-fold compared with controls, but had no effect on concentration of somatostatin in plasma. Relative to water-injected controls, blockade of 5-hydroxytryptaminergic receptors with cyproheptadine (0.2 mg/kg body wt, sc) decreased the area under growth hormone response curves for at least 110 min before feeding (71%) and after removal of feed (69%). The data support the hypothesis that 5-hydroxytryptaminergic receptors are involved in stimulation of pulsatile growth hormone secretion in meal-fed cattle. Lack of a change in concentration of somatostatin in plasma with respect to time of meal-feeding or after injection of the 5-hydroxytryptaminergic-receptor agonist quipazine suggests that 5-hydroxytryptaminergic receptor-stimulated growth hormone secretion is likely mediated within the central nervous system, rather than by meal-induced changes in peripheral secretion of somatostatin.

Animals↗

PubMed1995

Cannulation of a lateral ventricle in the brain of Holstein calves.

A surgical technique was developed for implanting a flexible polyurethane cannula in a lateral ventricle in the brain of calves. Initially, measurements were made on 25 calves at necropsy to develop equations for calculating coordinates for cannula placement. The distance (cm) caudal, in the sagittal plane, from the coronal suture line to the center of a hole to be drilled in the parietal bone of the skull was: 0.73 +/- (0.00925 x body weight [kg]). The distance (cm) lateral from the midline to the center of the hole to be drilled was: 0.018 +/- (0.6464 x distance caudal). The depth (cm) from the surface of the skull to the dorsal surface of the lateral ventricle was: 2.29 + (0.0159 x body weight [kg]). Surgery was subsequently performed on 17 calves. A 5-mm-diameter hole was drilled through the skull with a hand trephine at coordinates derived from the aforementioned regression equations. A polyurethane cannula (total length, 30 cm; 1 mm ID; 2 mm OD) covering a stainless-steel 20-gauge blunt-tipped needle (stylet) was lowered through the brain and into a lateral ventricle at an angle of 20.5 degrees relative to the frontal bones of the skull. The blunt-tipped needle was then removed, and CSF was allowed to drip from the cannula to verify placement. One stainless-steel screw was inserted 0.6 cm medial, and another was inserted 0.6 cm caudal to the hole in the skull. The area around the cannula, bone screws, and hole in the skull was covered with dental acrylic (approx 2 cm in diameter) to stabilize the cannula.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Protein and fat metabolism in cows given somavubove before parturition.

Forty-one Holstein cows were injected with 0, 5, or 14 mg/d of bST for the last 46 +/- 6 d before parturition. Compared with data for controls, the 5- and 14-mg doses of bST increased apparent protein synthesis about 16% before parturition. Exogenous bST before parturition increased apparent protein degradation 30% during wk 1 after parturition. During wk 1 of lactation, 14 mg of bST also increased milk protein yield 33%. No treatment differences were present in concentration of serum NEFA, body condition score, or thickness of subcutaneous fat. Therefore, administration of bST before parturition did not alter metabolism of subcutaneous fat. Prepartum treatment with 5 and 14 mg of bST increased and maintained serum somatotropin at 6.5 and 22.7 ng/ml, respectively, compared with 1.6 ng/ml in controls. Concentrations of serum IGF-I were initially increased but were not maintained as parturition approached. On d -23, IGF binding protein 3 was increased 65% but was not different among groups by d -7. For groups administered the 5 and 14 mg/d of bST, IGF binding protein 2 was decreased 40%. Administration of bST before parturition increased protein reserves and stimulated milk protein yield for 1 wk but did not alter metabolism of subcutaneous fat. Furthermore, energy balance appeared to be a major regulator of concentrations of IGF binding protein 3 and responsiveness of IGF-I to exogenous somatotropin before parturition.

Adipose Tissue↗

PubMed1994

Production responses of cows to recombinantly derived bovine somatotropin and to frequency of milking.

To determine whether bST additively increases milk production in cows milked at different frequencies per day, 118 Holstein primiparous and multiparous cows were milked two or three times daily beginning at parturition and received either 14 mg of bST or no injection beginning at d 75 of lactation. Increased milking frequency from two to three times daily increased 3.5% FCM in multiparous (4.7 kg/d) and primiparous (4.1 kg/d) cows over 305 d. Injection of bST increased FCM 4.3 kg/d in multiparous cows and 5.0 kg/d in primiparous cows over 230 d. Increased milking frequency from two to three times daily reduced milk fat and protein percentages in milk, but bST generally did not affect these percentages. Injection of bST prevented increases in body condition score as lactation advanced, but increasing milking frequency from two to three times daily did not. In general, bST and increased milking frequency additively increased FCM in multiparous and primiparous cows.

Animals↗