Flumethasone was given to Merino wethers weighing 30-50 kg at rates of 0·62-1· 35 mg/kgO' 7 5 by intravenous (experiments 1 and 2), intraruminal (experiment 4) and subcutaneous (experiment 5) routes over 8 days. In experiment 3, 1· 2 mgflumethasone/kg'"?" was given intravenously over 4, 5 or 6 days. The plasma concentration profiles showed concentrations in the order: intravenous > subcutaneous > intraruminal. Plasma concentration patterns usually were highest during the first 48 h of infusion followed by relatively stable values. This last feature was not evident in experiments when the rate of hormone infusion was increased. Estimates of the metabolic clearance rates for flumethasone in experiments 1, 2 and 5 were 200-700 ml/min during the' equilibrium concentration periods.The effects of flumethasone on some, aspects of wool growth revealed interactions between the routes of administration, the period of dosage and the rate of wool growth in the recipients.In experiments 1 and 2 intravenous infusion of 1·20-1· 33 mg flumethasone/kg'"?" caused the shedding of all wool fibres about 30 days after treatment. Some effects of dosing sheep with flumethasone at a time when wool growth was decreasing were also observed in experiment 2. Flumethasone given at a rate of 1· 2 mg/kg'"?" over 4, 5 or 6 days caused the shedding of only some wool fibres which were firmly retained on the sheep by the continuous fibres. Intraruminal and subcutaneous infusions of O·62-1· 35 mg flumethasone/kg'"?" had similar results to the last in the majority of animals although in a few cases no discontinuity of wool fibres was observed.Recovery in wool growth was observed after treatment. Animals regained their pretreatment wool growth in experiments 1, 4 and 5 by 60 days after treatment and probably equalled at that, time wool growth in controls. Recovery was retarded in some individuals in experiment 2 and in some groups in experiment 3. In experiment 1, 21 days wool growth was estimated to have been lost. Some aspects of complete versus partial shedding of wool fibres are discussed particularly with reference to wool harvesting. Some similarities in the appearance of fleeces of steroid-treated sheep and naturally shedding animals are also discussed.In some experiments, particularly when the infusion rate of flumethasone was increased (experiment 3), the sheep showed temporary but significant feed refusals during, but more commonly after, treatment. Speculative discussion as to the metabolic causes of this response is included.
Some effects of the parenteral administration of three glucocorticoid analogues, namely Opticortenol (dexamethasone-21 -trimethylacetate), Decadron phosphate (dexamethasone-21 -phosphate) and the heterocyclic corticosteroid, Cortivazol, were observed on wool growth in sheep. None of the glucocorticoids was satisfactory for defleecing sheep, principally because of variation between sheep and between body regions in the wool growth response. Four main types of response to dosing with glucocorticoids were observed : Firstly, with some animals there was no obvious effect on wool growth. In a second category there was a well-defined 'break' in some wool fibres but the fleece as a whole was retained by other unbroken fibres. Thirdly, complete or partial shedding of the fleece was seen, unshed portions usually being present on the head, neck and shoulder regions and consisting mainly of broken wool fibres but also a proportion of whole fibres. Finally, prolonged wool growth depression without shedding of the fleece during the experimental period was also seen. Results indicated that to obtain shedding of the fleece in 15-20 days after dosage, wool growth needs to be reduced below 20 per cent of its pre-treatment values and regrowth must be rapid.
Daily injection of a group of sheep with 75 mg. cortisol acetate (1.2 mg. per kilogram body weight) resulted in hyperglycemia and in a marked increase in plasma immunoreactive insulin concentrations. Doubling the dose of cortisol after fourteen days did not result in further increases in glucose or insulin concentrations, but the elevated levels were maintained throughout treatment. Intravenous glucose tolerance tests using 0.1 gm. glucose per kilogram body weight showed that the rate of glucose removal was decreased and the increment in plasma insulin concentration reduced by cortisol treatment. With a larger glucose load (0.5 gm. per kilogram body weight) there was an exaggerated insulin response to the increased plasma glucose level during the first period of cortisol treatment, but in the second period the response was no greater than that in the control period. Changes in plasma glucose and insulin concentrations in the eight hours following feeding were much exaggerated during cortisol treatment, even though there is little absorption of glucose from the digestive tract in this species.In the absence of evidence of increased glucose turnover in the sheep during cortisol-induced hyperglycemia, the changes are indicative of marked impairment of peripheral glucose metabolism and antagonism of insulin action by cortisol in this species. DIABETES 76:566-71, August, 1967. Since the observation by Long, Katzin, and Fry 1 that the blood glucose concentration of normal or partially depancreatized rats was increased by treatment with adrenal steroids, effects of the glucocorticoid hormones on carbohydrate metabolism and on pancreatic islet cell morphology have been widely studied. The work in these fields has recently been reviewed in detail by Haist. 2 However, while changes in the islets suggest increased insulin secretion, 3 the effects of glucocorticoid hormones on peripheral plasma insulin concentrations have received little attention.In the sheep, hyperglycemia usually accompanies elevated plasma cortisol concentrations, 4 ' 6 but despite this positive association between glucose and cortisol concentrations we have obtained no evidence to suggest that the hyperglycemia is maintained by high rates of glucose production. 6 In view of the changes in pancreatic islet size and structure which occur during hyperadrenocorticism in other species, 3 * 7 " 9 it seemed likely that plasma insulin concentration in the sheep would be influenced markedly by cortisol treatment. The observations reported here show that plasma insulin concentration increases during the hyperglycemia produced by cortisol treatment and the results give added support to the view that cortisol seriously antagonizes peripheral glucose metabolism. MATERIALS AND METHODSEight adult Border Leicester x Merino crossbred female sheep (body weight 62.5 db 1.3 kg.), thoroughly trained to the procedures involved, were used in the experiments. They were housed individually in pens and were fed 8po gm. daily of a diet consisting of equal parts of chaffed lucerne...
The patterns of plasma concentrations of thyroxine (T4), triiodothyronine (T3) and cholesterol were determined in tropically adapted (ZX) and temperate (SH) breeds of cattle in the first 6 days of their lives in a tropical environment. T4 concentrations were high at birth and fell to within normal adult values at 6 days of age. In contrast, plasma cholesterol levels were low at birth and increased daily to the highest values on day 6. T3 levels increased from birth to maximum values at 12 h after birth and then declined progressively. The T4/T3 molar ratios were high at birth and decreased to lower values on day 2. T4 and cholesterol levels were higher (p < 0.001) in ZX than in SH calves, and in calves born in winter were higher (p < 0.001) in females than in males. There were significant (p < 0.001) animal within-breed differences in all parameters. The results are discussed with reference to the use of physiological and biochemical indices for the early selection of cattle suited to tropical conditions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.