Adrenocortical functions in a macropodid marsupial Thylogale billardierii

1986 ◽  
Vol 110 (3) ◽  
pp. 471-480 ◽  
Author(s):  
I. K. Martin ◽  
I. R. McDonald

ABSTRACT In a study of adrenocortical functions in macropodid marsupials, measurements were made of the effects of ACTH infusion, ether stress and adrenaline infusion on plasma corticosteroid and glucose concentrations in wallabies (Thylogale billardierii) provided with indwelling venous catheters. The mean plasma total glucocorticoid concentration in undisturbed males and females was 80 ± 5 (s.e.m.) μg/l, of which more than 90% was cortisol. This fraction declined to 68% of the total at the highest ACTH-stimulated concentration of 225 μg/l, due to an increase in the contribution by 11-deoxycortisol. Although maximal ACTH stimulation (4·5 i.u./kg per h) caused a five- to sixfold increase in cortisol secretion rate, as measured by isotope dilution during constant-rate tracer infusion, plasma cortisol concentration rose only two- to threefold, due to a marked increase in metabolic clearance. Plasma glucose concentration did not change significantly during either short-term (1 h) i.v. infusion or long-term (8 days) i.m. injection of ACTH, even though plasma cortisol concentration was significantly increased. Ether anaesthesia caused a marked hyperglycaemia that preceded an increase in plasma cortisol concentration and was not sustained while plasma cortisol concentration continued to increase. Infusion of adrenaline i.v. at rates sufficient to cause a similar hyperglycaemia had no significant effect on plasma cortisol concentration. A marked hyperglycaemia during xylazine anaesthesia was not associated with an increase in plasma cortisol concentration and was attributable to suppression of insulin secretion. It is concluded that, as in the red kangaroo (Macropus rufus) and the quokka (Setonix brachyurus) and in contrast to the reported effects in the tammar wallaby (Macropus eugenii), neither ACTH, nor the increase in plasma glucocorticoid concentration caused by ACTH administration, influence plasma glucose concentration in Thylogale billardierii. J. Endocr. (1986) 110, 471–480

2003 ◽  
Vol 13 (4) ◽  
pp. 436-453 ◽  
Author(s):  
Graeme I. Lancaster ◽  
Roy L.P.G. Jentjens ◽  
Luke Moseley ◽  
Asker E. Jeukendrup ◽  
Michael Gleeson

The purpose of the present study was to examine the effect of pre-exercise carbohydrate (CHO) ingestion on circulating leukocyte numbers, plasma interleukin (IL)-6, plasma cortisol, and lipopolysaccharide (LPS)-stimulated neutrophil degranulation responses in moderately trained male cyclists who completed approximately 1-h of high-intensity cycling. The influence of the timing of pre-exercise CHO ingestion was investigated in 8 subjects who consumed 75 g CHO as a glucose solution at either 15 (–15 trial), or 75 (–75 trial) min before the onset of exercise. The influence of the amount of pre-exercise CHO ingestion was investigated in a further 10 subjects who consumed either 25 g or 200 g CHO as a glucose solution or a placebo 45 min before the onset of exercise. At the onset of exercise in the timing experiment, the plasma glucose concentration was significantly (p < .05) lower on the –75 trial compared with pre-drink values, and the plasma cortisol concentration and neutrophil to lymphocyte (N/L) ratio were significantly (p < .05) elevated in the post-exercise period. In the –15 trial, plasma glucose concentration was well maintained, and the plasma cortisol concentration and N/L ratio were not significantly elevated above resting levels. However, LPS-stimulated neutrophil degranulation was similar in the –15 and –75 trials. The amount of CHO ingested had no effect on the magnitude of the rise in the N/L ratio compared with placebo when consumed 45 min pre-exercise. Finally, although an exercise-induced increase in the plasma IL-6 concentration was observed, this effect was independent of pre-exercise CHO ingestion.


1995 ◽  
Vol 82 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Dounia Sbai ◽  
Philippe Jouvet ◽  
Anne Soulier ◽  
Luc Penicaud ◽  
Jacques Merckx ◽  
...  

Background It should be possible to avoid variations in plasma glucose concentration during anesthesia by adjusting glucose infusion rate to whole-body glucose uptake. To study this hypothesis, we measured glucose utilization and production, before and during halothane anesthesia. Methods After an overnight fast, six adolescents between 12 and 17 yr of age were infused with tracer doses of [6,6-2H2]glucose for 2 h before undergoing anesthesia, and the infusion was continued after induction, until the beginning of surgery. Plasma glucose concentration was monitored throughout, and free fatty acids, lactate, insulin, and glucagon concentrations were measured before and during anesthesia. Results Despite the use of a glucose-free maintenance solution, plasma glucose concentration increased slightly but significantly 5 min after induction (5.3 +/- 0.4 vs. 4.5 +/- 0.4 mmol.l-1, P &lt; 0.05). This early increase corresponded to a significant increase in endogenous glucose production over basal conditions (4.1 +/- 0.4 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P &lt; 0.05), with no concomitant change in peripheral glucose utilization. Fifteen minutes after induction, both glucose utilization and production rates decreased steadily and were 20% less than basal values by 35 min after induction (2.9 +/- 0.3 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P &lt; 0.05). Similarly, glucose metabolic clearance rate decreased by 25% after 35 min. Despite the increase in blood glucose concentration, anesthesia resulted in a significant decrease in plasma insulin concentration. Conclusions These data suggest that halothane anesthesia per se affects glucose metabolism. The decrease in peripheral glucose utilization and metabolic clearance rates and the blunted insulin release question the relevance of glucose infusion in these clinical settings.


Author(s):  
R.G. Lobetti

A 9-year-old male German shepherd dog was evaluated for clinical and clinico-pathological changes that were suggestive of Addison's disease. On further investigation the basal plasma cortisol concentration was high, a normal cortisol response to ACTH stimulation occurred, plasma renin activity was elevated and low serum aldosterone concentration was present. A diagnosis of hyperreninaemic hypoaldosteronism was made. Replacement fludrocortisone resulted in complete normalisation of the electrolyte and fluid imbalances. Hyperreninaemic hypoaldosteronism has never been reported in the dog.


1994 ◽  
Vol 267 (5) ◽  
pp. R1226-R1234 ◽  
Author(s):  
T. G. West ◽  
C. J. Brauner ◽  
P. W. Hochachka

The involvement of circulatory glucose in the energy provision of skeletal muscle and heart of swimming carp was examined. Plasma glucose concentration varied from 3 to 17 mM among individual carp, and estimates of glucose turnover rate (RT) were positively correlated with plasma glucose level in resting fish (range 1.6-6.3 mumol.min-1.kg-1) and in swimming fish (range 4.2-10.7 mumol.min-1.kg-1). Carp that were exercised at 80% of their critical swimming speed displayed a twofold higher RT at any given plasma glucose concentration. Metabolic clearance rate also doubled in swimming carp (1.0 +/- 0.1 ml.min-1.kg-1) relative to resting controls (0.5 +/- 0.1 ml.min-1.kg-1). Indexes of muscle glucose utilization (GUI), determined with 2-deoxy-D-[14C]glucose, indicated that glucose utilization in red muscle was not dependent on plasma glucose concentration; however, glucose utilization in this muscle mass was threefold higher in swimming fish than in resting control fish. On the basis of whole body aerobic scope measurements in carp, it was estimated that circulatory glucose potentially comprised 25-30% of the total fuel oxidation in the active red muscle mass. GUI in heart was positively correlated with plasma glucose concentration, and it is possible that glucose availability had considerable influence on the pattern of myocardial substrate oxidation in resting and active carp. Carp are somewhat more reliant than rainbow trout on glucose for locomotor energetics, correlating with species differences in swimming capability and with the greater capacity of omnivorous carp to tolerate dietary glucose.


2010 ◽  
Vol 112 (5) ◽  
pp. 1204-1210 ◽  
Author(s):  
Armelle Nicolas-Robin ◽  
Jérome D. Barouk ◽  
Julien Amour ◽  
Pierre Coriat ◽  
Bruno Riou ◽  
...  

Background Hemodynamic instability is frequent in brain-dead patients and may result, in part, from absolute or relative adrenal insufficiency. Corticosteroid supplementation is widely used to restore hemodynamic stability in septic shock and to reduce the time of shock resolution. The authors verified that supplementation with hydrocortisone may enhance hemodynamic stability in brain-dead patients. Methods All consecutive brain-dead patients with hypotension requiring vasopressor agents were included in this single-center noninterventional clinical observation study. Assessment of baseline and adrenocorticotropic hormone (ACTH)-stimulated plasma cortisol concentrations was performed. Immediately after, patients were systematically treated with a single intravenous injection of hydrocortisone (50 mg), and norepinephrine administration was adjusted every 15 min to maintain mean arterial pressure between 65 and 90 mmHg. Adrenal insufficiency was defined as baseline plasma cortisol concentration less than 15 microg/dl and/or delta plasma cortisol concentration less than 9 microg/dl. Patients were considered as ACTH responders when delta cortisol concentration was more than 9 microg/dl 30 min after ACTH injection. Results Among the 31 patients included, the incidence of adrenal insufficiency was 87% [95% CI, 70-96%]. A significant (&gt; or =30%) decrease in norepinephrine dose was obtained 180 min after hydrocortisone injection in 18 (59%) patients, from 0.31 [0.16-0.44] microg . kg(-1) . min(-1) to 0.18 [0.10-0.24] microg . kg(-1) . min(-1) (P &lt; 0.01). The incidence of hemodynamic response was greater in ACTH nonresponders than in ACTH responders: 86% versus 50%, respectively, P &lt; 0.05. Conclusions Adrenal insufficiency with hemodynamic instability is frequent in brain-dead patients. After ACTH stimulation testing and hydrocortisone infusion, hemodynamic stability is enhanced especially in patients with true adrenal nonfunction.


1994 ◽  
Vol 72 (10) ◽  
pp. 1826-1830 ◽  
Author(s):  
P. J. Goddard ◽  
S. M. Rhind ◽  
W. J. Hamilton ◽  
A. J. Macdonald ◽  
A. R. Fawcett ◽  
...  

The adrenocorticotrophic hormone (ACTH) stimulation test was assessed in red deer (Cervus elaphus). Following injection (i.v.) of 0, 100, 250, or 500 μg synthetic ACTH in farmed hinds (5 per group; mean live mass 78 kg), peak plasma cortisol concentrations occurred 30 min later. There was no dose effect on the peak levels attained, but the duration of the response increased with dose. The response of wild hinds (mean live mass 64 kg) to 500 μg ACTH administered at the time of capture was studied. Plasma cortisol concentrations were high prior to ACTH administration (238 ± 17.6 nmol/L; mean ± SE). Eighty minutes later, although concentrations were lower overall, they were significantly higher in ACTH-treated than in control animals (21 per group). Twenty farmed male red deer calves (aged 5 months at the outset; mean live mass 44 kg) were permanently housed after weaning. One hundred micrograms of ACTH was injected at weeks 0 (just after weaning) and 12. At week 12 mean cortisol concentrations were lower both before and after ACTH injection, although ACTH significantly increased plasma cortisol concentration on both occasions. Together these experiments suggest that the ACTH stimulation test can be employed in some classes of red deer but that it is not appropriate when animals have a high initial plasma cortisol concentration.


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