Plasma cortisol concentrations following cortisone infusion in dogs before and after treatment with cortisone acetate

OBJECTIVE: To evaluate effects of iatrogenic hyperadrenocorticism on plasma cortisol concentrations produced by an infusion of hydrocortisone in dogs. PROCEDURE: Plasma cortisol concentrations were measured regularly during a 6 h infusion of hydrocortisone sodium succinate at two dose rates. The infusions were performed before and after treatment for 30 d with oral cortisone acetate at 10 mg/kg/24 h, divided thrice daily. Adrenal activity during the experimental period was assessed by weekly ACTH stimulation tests. RESULTS: Both infusion rates produced lower plasma cortisol concentrations after treatment for 30 d with cortisone. CONCLUSION: Prior exposure to high concentrations of glucocorticoids may result in accelerated metabolism of glucocorticoids administered subsequently. This may necessitate increased dosages when using glucocorticoids to support inadequate adrenal function.     

Effects of delmadinone acetate on pituitary-adrenal function, glucose tolerance and growth hormone in male dogs

Objective To characterise the effects of delmadinone acetate on the pituitary-adrenal axis, glucose tolerance and growth hormone concentration in normal male dogs and dogs with benign prostatic hyperplasia.
Design A prospective study involving nine normal male dogs and seven with prostatic hyperplasia.
Procedure Delmadinone acetate was administered to six normal male dogs and seven dogs with benign prostatic hyperplasia at recommended dose rates (1.5 mg/kg subcuta-neously at 0, 1 and 4 weeks). Three normal controls received saline at the same intervals. Blood concentrations of ACTH, cortisol, glucose, insulin and growth hormone were measured over 50 days. Intravenous glucose tolerance and ACTH response tests were performed before and after treatment in the nine normal animals.
Results A substantial suppression of basal and 2 h post-ACTH plasma cortisol secretion was demonstrated after one dose in all dogs given delmadinone acetate. Individual responses after the second and third administration varied between recovery in adrenal responsiveness to continued suppression. Plasma ACTH concentration was also diminished after one treatment. No effects were evident on glucose tolerance or serum growth hormone concentrations.
Conclusion Delmadinone acetate causes adrenal suppression from inhibition of release of ACTH from the pituitary gland. Treated dogs may be at risk of developing signs of glucocorticoid insufficiency if subjected to stressful events during or after therapy. Neither glucose intolerance nor hyper-somatotropism seems likely in male dogs given delmadinone acetate at the recommended dose rate, but the potential for excessive growth hormone secretion in treated bitches remains undetermined.     

Effect of chronic hypocortisolaemia on plasma cortisol concentrations during intravenous infusions of hydrocortisone sodium succinate in dogs

Intravenous infusions of hydrocortisone sodium succinate (HSS) were given at 0·625 mg kg⁻¹ hour⁻¹ and 0·312 mg kg⁻¹ hour⁻¹ to six dogs. Plasma cortisol concentrations were measured by radioimmunoassay at 0, 15, 30, 45 and 60 minutes and then every 30 minutes for a further five hours. Chronic hypocortisolaemia was induced and maintained with mitotane and the HSS infusions were repeated after 31 and 50 days. No statistically significant difference was observed in the plasma cortisol concentrations after either period of hypocortisolaemia, but the plasma cortisol concentrations tended to be higher in most of the dogs.     

Effect of cortisol infusion patterns and castration on metabolic and immunological indices of stress response in cattle

This study tested the hypotheses that: (1) either acute stress induced by Burdizzo castration, or cortisol infusion would modulate plasma glucose, insulin and growth hormone (GH) concentrations; and (2) immune modulation induced by cortisol would be dependent on the pattern, intensity and duration of circulating cortisol concentrations. Fifty 9.2-month-old Holstein×Friesian bulls (232±2.0 kg) were blocked by weight and randomly assigned to one of five treatments (n=10 per treatment): (1) sham handled control; (2) Burdizzo castration; (3) hydrocortisone infusion to mimic the castration-induced secretion pattern of cortisol; (4) hourly pulse infusion of hydrocortisone; and (5) sustained infusion of hydrocortisone for 8 h. Blood samples were collected intensively on day 0, and weekly from days 1 to 35. Castration acutely increased plasma cortisol, GH and haptoglobin concentrations, suppressed lymphocyte in vitro interferon-γ (IFN-γ) production, but had no effect on plasma glucose and insulin concentrations. Cortisol infusion to simulate the castration-induced secretion pattern of cortisol, and pulse infusion of cortisol did not suppress the IFN-γ production. A sustained infusion of cortisol resulted in the transient suppression of IFN-γ production. Moreover, the sustained cortisol infusion resulted in increased plasma glucose, insulin and GH concentrations. The overall 14-day feed intakes and 35-day growth rates were not affected by treatments. In conclusion, cortisol infusion to induce immune suppression in vivo occurred only at pharmacological doses. Within physiological ranges, cortisol was not associated with the suppression of immune function, indicating that during castration cortisol per se is not responsible for the suppression of in vitro IFN-γ production.     

Plasma cortisol responses to three cortico-trophic preparations in normal dogs

Objective To compare cortisol responses to three corticotrophic preparations in normal dogs.
Animals Eight clinically normal dogs (four intact males, four intact females) of medium size.
Procedures Each dog received four treatments on four separate occasions in a duplicated Latin square pattern. Treatments were two adrenocorticotrophin (ACTH) preparations given intramuscularly at 2.2 U/kg, one of the ACTH preparations given intramuscularly at 1 U/kg and a synthetic polypeptide with ACTH-like activity (tetracosactrin, cosyntropin) given intravenously at 5 μg/kg. Plasma samples were taken for cortisol assay before and at 0.5, 1, 2 and 4 h after treatment.
Results Plasma cortisol concentrations were similar with the two ACTH preparations and at both dose rates. Tetracosactrin produced smaller mean peak cortisol concentrations, which tended to occur earlier than with ACTH, and smaller values for the area under the curve of plasma cortisol concentration from zero time to 4 h.
Conclusion The findings suggest that canine adrenal function can be tested adequately by giving ACTH intramuscularly at 1 U/kg and measuring plasma cortisol in samples taken at 0 and 2 h, or by giving tetracosactrin intravenously at 5 μg/kg and determining cortisol concentration at 0 and 1 h.     

The effects of 10% hypertonic saline, 0.9% saline and hydroxy ethyl starch infusions on hydro-electrolyte status and adrenal function in healthy conscious dogs

The purpose of this study was to investigate the influence of different saline and colloid solutions on adrenal steroid secretion in dogs. Six healthy male Beagles underwent three infusion cycles: 10 min infusion of 30 ml/kg of NaCl 0.9%, 5 ml/kg of hydroxy ethyl starch, or 5 ml/kg of NaCl 10%. Plasma osmolality, hematocrit, total solids, cortisol and aldosterone levels were measured at 0, 5, 15, 30, 60, 120, 180 and 240 min after beginning infusion. Plasma ACTH levels were measured at 0, 15 and 240 min. An identical timing of sampling was applied during a control session omitting the fluid infusion. Osmolality, sodium, chloride and cortisol levels were found to be significantly higher with hypertonic saline solute compared to control. All fluid infusions lead to lowered plasma potassium, hematocrit, total solids and aldosterone values. ACTH concentrations did not show significant changes with any of the infusion cycles. The increase in cortisol levels suggests that hypertonic saline infusion could be interesting in critical care resuscitation, particularly in patients who are suffering from relative adrenal insufficiency.     

Does cortisol inhibit vasopressin secretion in sheep?

Glucocorticoids inhibit the plasma vasopressin responses to hemorrhage and hypoxia in dogs. Attempts to demonstrate glucocorticoid inhibition of vasopressin secretion in fetal sheep have been unsuccessful, suggesting the possibility that there is an influence of development on the expression of this interaction, or that the interaction cannot be demonstrated in all mammalian species. This study was designed to investigate these two possibilities. Adult ewes chronically prepared with carotid arterial loops, were subjected to 5 hr infusions of cortisol at a rate of 6 ug/kg min or vehicle (5% ethanol in saline). The infusion of cortisol increased plasma cortisol concentration from 26 +/- 3 to 46 +/- 8 ng/ml, while vehicle infusion was associated with a decrease in plasma cortisol concentration from 23 +/- 4 to 15 +/- 3 ng/ml. One hr after the end of the cortisol or vehicle infusions, vasopressin secretion was stimulated by arterial hypotension produced by 10 min infusions of sodium nitroprusside (20 ug/kg min). Nitroprusside decreased arterial blood pressure equally in both groups. Plasma vasopressin concentrations were increased to peak concentrations of 92 +/- 33 and 116 +/- 20 pg/ml in the vehicle- and cortisol-infused groups, responses which were not significantly different as tested by ANOVA. We conclude that increases in plasma cortisol concentration, equal to those observed during responses to stressors, do not inhibit vasopressin secretion in this species.     

Effects of synthetic ovine corticotropin-releasing hormone on plasma concentrations of immunoreactive adrenocorticotropin, alpha-melanocyte-stimulating hormone, and cortisol in dogs with naturally acquired adrenocortical insufficiency.

We evaluated the effect of ovine corticotropin-releasing hormone (CRH) on plasma immunoreactive (IR) concentrations of ACTH, alpha-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma IR-ACTH concentrations, which failed to increase after administration of CRH. Basal plasma alpha-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by CRH administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of CRH. Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma IR-ACTH concentrations and exaggerated responses to CRH, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of IR-ACTH that did not increase after stimulation with CRH.     

Combined dexamethasone suppression and cosyntropin (synthetic ACTH) stimulation test in the dog: new approach to testing of adrenal gland function

A combined dexamethasone suppression and cosyntropin (synthetic ACTH) stimulation test was developed in the dog so that information concerning pituitary gland (hypophysis) and adrenal gland competence could be provided in a single trial, during a short time span. Treatment of dogs with dexamethasone (0.1 mg/kg, IM) resulted in total suppression (below assay sensitivity or < 10 ng/ml) of plasma hydrocortisone (cortisol) at postinjection hour (PIH) 2 in 100% of the dogs, whereas suppression was inconsistent at PIH 1. Cosyntropin (0.5 U/kg, IV) administration to normal or dexamethasone-suppressed dogs increased plasma hydrocortisone concentration 3.5 to 4.5 times base-line values at PIH 1, which was the time of maximal effect. The combined test concept for adrenal gland function is valid, convenient (three sample collections; 3-hour period), and allows testing of adrenal gland response to dexamethasone suppression and ACTH stimulation in a single trial. The following test procedure for dogs is recommended: (i) collect base-line plasma sample (0900 hours) followed by injection of dexamethasone (0.1 mg/kg, IM); (ii) collect second plasma sample 2 hours after dexamethasone (to evaluate suppression of plasma hydrocortisone concentration) followed by the injection of cosyntropin (0.5 U/kg, IV); and (iii) collect a third plasma sample 1 hour later to evaluate plasma hydrocortisone concentration after cosyntropin stimulation.     

Canine plasma cortisol (hydrocortisone) measured by radioimmunoassay: clinical absence of diurnal variation and results of ACTH stimulation and dexamethasone suppression tests.

A radioimmunoassay for plasma cortisol (hydrocortisone) was developed and validated for sensitivity, specificity, accuracy, precision, and parallelism. Steroids were extracted with ethyl ether, and cortisol was purified by gel column chromatography prior to assay. [1,2-3H] cortisol and a commercially available sheep antibody to cortisol-21-hemisuccinate were used. Free steriods were separated from bound steroids by centrifugation after adsorption to dextran-coated charcoal. Plasma cortisol was measured by this technique in 6 normal dogs. Circadian rhythm of cortisol secretion was not detected in samples obtained by venipuncture at 8 different hours on 3 separate days, suggesting that adrenal function tests may be started in clinical patients at any time of day. Resting plasma cortisol concentrations averaged 19.4+/-3.0 (SD) ng/ml and ranged from nondetectable (less than 3 ng/ml) to 77.5 ng/ml. Of 144 canine plasma samples, 95% contained less than 50 ng of cortisol/ml. Intramuscular injection of 2.2 units of adrenocorticotropic hormone/kg of body weight caused detectable increase in plasma cortisol concentrations; maximum response (68.3 to 111.6 ng/ml) occurred 1 to 2 hours after injection. Oral administration of dexamethasone suppressed plasma cortisol to nondetectable concentrations for 32 hours in all 6 dogs.     

Lymphoma as a model for chronic illness: effects on adrenocortical function testing

Many dogs with chronic illness have serum biochemical abnormalities consistent with hyperadrenocorticism (HAC). Lymphoma (LSA) is a chronic disease of dogs. The purpose of this study was to evaluate adrenocortical screening test results in dogs with LSA to evaluate their specificity. Criteria for inclusion in the study included a diagnosis of LSA, an expected survival time of 16-56 weeks, no glucocorticoid treatment beyond 4 weeks after the initiation of chemotherapy, no evidence of HAC, and owner consent. Post-ACTH stimulation plasma cortisol concentrations (PACs), urine cortisol : creatinine (UC : Cr) ratios, and maximal left adrenal width measurements were performed at the time of LSA diagnosis before the initiation of chemotherapy and at 16, 24, 32, 40, and 52 weeks or until the loss of remission or the development of another disease. Ten dogs met the criteria for inclusion. Forty-two PACs were performed; 1 abnormal, 2 borderline, and 39 normal values were detected. Thirty-five maximal left adrenal width measurements were obtained; 0 abnormal, 5 borderline, and 30 normal measurements were detected. Thirty-six UC : Cr ratios were obtained, with 26 abnormal, 4 borderline, and 6 normal values detected and 9 of 10 dogs having at least 1 abnormal value. These data suggest that in dogs with LSA, the UC : Cr ratio frequently is abnormal and may not be a specific test for HAC, or it may be the most sensitive test for increases in cortisol secretion due to chronic illness. Maximal left adrenal width measurements and PACs were almost always normal and may be more specific for HAC or less sensitive for demonstrating chronic increases in cortisol secretion.     

Influence of aging on adrenal responsiveness in a population of eleven healthy beagles

The present study aimed at investigating the effects of aging on the adrenal cortex response of cortisol and aldosterone in dogs.A population of healthy adult Beagles was evaluated twice at a five-year interval. At each evaluation, plasma basal cortisol and aldosterone, cortisol and aldosterone following ACTH-stimulation, sodium, and potassium concentrations and arterial blood pressure were measured. We observed significantly (p < 0.05) greater sodium, urea and creatinine concentrations with aging. Nevertheless urea and creatinine remained within our laboratory reference ranges. This study showed a highly significant age-related elevation of basal cortisol (p < 0.01). Inversely, both aldosterone following ACTH-stimulation levels and difference between aldosterone following ACTH-stimulation and basal aldosterone values plummeted significantly (p < 0.01) with aging. In conclusion, the evaluation of the adrenal cortex function in dogs should take in consideration the age of the individuals.     

The effects of 10% hypertonic saline, 0.9% saline and hydroxy ethyl starch infusions on hydro-electrolyte status and adrenal function in healthy conscious dogs

The purpose of this study was to investigate the influence of different saline and colloid solutions on adrenal steroid secretion in dogs. Six healthy male Beagles underwent three infusion cycles: 10 min infusion of 30 ml/kg of NaCl 0.9%, 5 ml/kg of hydroxy ethyl starch, or 5 ml/kg of NaCl 10%. Plasma osmolality, hematocrit, total solids, cortisol and aldosterone levels were measured at 0, 5, 15, 30, 60, 120, 180 and 240 min after beginning infusion. Plasma ACTH levels were measured at 0, 15 and 240 min. An identical timing of sampling was applied during a control session omitting the fluid infusion. Osmolality, sodium, chloride and cortisol levels were found to be significantly higher with hypertonic saline solute compared to control. All fluid infusions lead to lowered plasma potassium, hematocrit, total solids and aldosterone values. ACTH concentrations did not show significant changes with any of the infusion cycles. The increase in cortisol levels suggests that hypertonic saline infusion could be interesting in critical care resuscitation, particularly in patients who are suffering from relative adrenal insufficiency.     

Restitution of blood volume after hemorrhage in dogs with adrenocortical suppression

Groups of splenectomized dogs were treated with weekly im doses of a potent glucocorticoid, methylprednisolone acetate (MPA; 2.5 mg/kg) or MPA-vehicle (controls) to determine if glucocorticoid-induced adrenocortical suppression would alter the restitution of blood volume in response to a 7.5 ml/kg hemorrhage. Five of the MPA-treated dogs were infused with cortisol (17 μg/min) for 2 hr beginning with the onset of hemorrhage. Blood volume restitution at 24 hr post-hemorrhage was reduced (P<0.05) in MPA-treated (46.5 ± 4.7%) or MPA-treated- cortisol infused (69.8 ± 9.7%) dogs as compared to controls (114 ± 11.8%). Hemorrhage was associated with a rapid increase in plasma immunoreactive (i) ACTH and cortisol concentrations in controls. In contrast, MPA treatment lowered baseline plasma iACTH and cortisol concentrations and prevented increases in either hormone following hemorrhage. Infusion of cortisol in one group of MPA-treated dogs gradually raised plasma cortisol concentrations but to lower (P<0.05) concentrations than measured in controls. Plasma aldosterone and glucose concentrations were not altered by MPA-treatment. Plasma osmolality increased to a greater (P<0.05) extent after hemorrhage in controls than in either group of MPA-treated dogs. It is concluded that glucocorticoid-induced adrenocortical suppression impairs the normal blood volume restitution process after moderate hemorrhage. The failure of cortisol infusion to fully restore restitution after MPA treatment may indicate that the pattern of the plasma cortisol response to hemorrhage is important in activating the restitution process or that MPA treatment diminishes non-cortisol dependent factors involved in restitution.     

Aldosterone-to-renin and cortisol-to-adrenocorticotropic hormone ratios in healthy dogs and dogs with primary hypoadrenocorticism

In dogs with primary hypoadrenocorticism, hypocortisolism and hypoaldosteronism usually are present, but these deficiencies also may occur in isolated forms. The diagnosis is commonly made by measuring plasma cortisol concentration before and after stimulation with ACTH, thereby ignoring aldosterone. In search of an alternative approach that would include assessment of glucocorticoid and mineralocorticoid production, 2 pairs of endocrine variables were measured: (1) plasma concentration of cortisol and ACTH, and (2) plasma aldosterone concentration and plasma renin activity. In addition, the cortisol-to-ACTH ratio (CAR) and the aldosterone-to-renin ratio (ARR) were calculated. Reference intervals were established in a population of 60 healthy dogs. In these dogs, CAR ranged from 1.1 to 26.1 and ARR ranged from 0.1 to 1.5. The variables were compared with those of 22 dogs with spontaneous primary hypoadrenocorticism. Plasma concentration of cortisol and ACTH in both groups of dogs overlapped, whereas CAR did not. Similarly, plasma aldosterone concentration and plasma renin activity overlapped, whereas ARR did not. These observations indicate that measurement of these endogenous variables (in one blood sample) allows the specific diagnoses of primary hypocortisolism and primary hypoaldosteronism.     

Measurement of plasma chromogranin A concentrations for assessment of stress responses in dogs with insulin-induced hypoglycemia

OBJECTIVE: To determine whether cross-reactivity exists between canine chromogranin A (CgA) and anti-human CgA antibody and investigate the usefulness of plasma CgA concentration measurements as an index of acute stress responses in dogs. ANIMALS: 12 healthy Beagles. PROCEDURE: Canine CgA was extracted and purified from canine adrenal glands of cadaver dogs for studying cross-reactivity with anti-human CgA antibody. Western blotting with anti-human CgA antibody was performed. Blood samples were collected from dogs at 0, 10, 20, 30, 40, 60, 120, and 180 minutes after IV administration of saline (0.9% NaCl) solution or insulin. Canine plasma CgA concentrations were determined by use of a CgA ELISA kit with rabbit antiserum against the carboxy-terminal fragment of human CgA. Plasma cortisol and catecholamine (ie, norepinephrine and epinephrine) concentrations were measured by use of an ELISA and a high-performance liquid chromatography method, respectively. RESULTS: Purified canine CgA was specifically detected by use of western blot analysis and an ELISA with anti-human CgA antibody. An increase in plasma CgA concentrations was observed in insulin-induced hypoglycemic dogs. Changes in plasma CgA concentration were correlated with changes in plasma cortisol or catecholamine concentrations of hypoglycemic dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Use of the CgA ELISA kit for determination of human plasma CgA concentrations is applicable to the measurement of canine plasma CgA concentrations. Canine plasma CgA concentrations, along with measurements of plasma cortisol and catecholamine concentrations, correctly reflect insulin-induced hypoglycemic stressed conditions in dogs. Measurement of canine plasma CgA concentrations may provide a useful index for evaluation of an acute stress response.     

Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005)

OBJECTIVE: To determine whether basal serum or plasma cortisol concentration can be used as a screening test to rule out hypoadrenocorticism in dogs. DESIGN: Retrospective case-control study. ANIMALS: 110 dogs with nonadrenal gland illnesses and 13 dogs with hypoadrenocorticism. PROCEDURES: Sensitivity and specificity of basal serum or plasma cortisol concentrations of either 2 microg/dL that are not receiving corticosteroids, mitotane, or ketoconazole are highly unlikely to have hypoadrenocorticism. However, if the basal cortisol concentration is 相似文献   

Evaluation of a low-dose synthetic adrenocorticotropic hormone stimulation test in clinically normal dogs and dogs with naturally developing hyperadrenocorticism.

OBJECTIVE: To determine whether low doses of synthetic ACTH could induce a maximal cortisol response in clinically normal dogs and to compare a low-dose ACTH stimulation protocol to a standard high-dose ACTH stimulation protocol in dogs with hyperadrenocorticism. DESIGN: Cohort study. ANIMALS: 6 clinically normal dogs and 7 dogs with hyperadrenocorticism. PROCEDURE: Each clinically normal dog was given 1 of 3 doses of cosyntropin (1, 5, or 10 micrograms/kg [0.45, 2.3, or 4.5 micrograms/lb] of body weight, i.v.) in random order at 2-week intervals. Samples for determination of plasma cortisol and ACTH concentrations were obtained before and 30, 60, 90, and 120 minutes after ACTH administration. Each dog with hyperadrenocorticism was given 2 doses of cosyntropin (5 micrograms/kg or 250 micrograms/dog) in random order at 2-week intervals. In these dogs, samples for determination of plasma cortisol concentrations were obtained before and 60 minutes after ACTH administration. RESULTS: In the clinically normal dogs, peak cortisol concentration and area under the plasma cortisol response curve did not differ significantly among the 3 doses. However, mean plasma cortisol concentration in dogs given 1 microgram/kg peaked at 60 minutes, whereas dogs given doses of 5 or 10 micrograms/kg had peak cortisol values at 90 minutes. In dogs with hyperadrenocorticism, significant differences were not detected between cortisol concentrations after administration of the low or high dose of cosyntropin. CLINICAL IMPLICATIONS: Administration of cosyntropin at a rate of 5 micrograms/kg resulted in maximal stimulation of the adrenal cortex in clinically normal dogs and dogs with hyperadrenocorticism.     

Assessment of the metabolic effects of hydrocortisone on llamas before and after feed restriction

OBJECTIVE: To evaluate the effects of administration of hydrocortisone on plasma concentration of insulin and serum concentrations of glucose, triglyceride, and nonesterified fatty acids (NEFAs) in llamas before and after feed restriction. ANIMALS: 9 adult female llamas. PROCEDURE: Feed was withheld from llamas for 8 hours. Blood samples were collected before (0 minutes) and 120, 180, 240, and 300 minutes after IV injection of hydrocortisone sodium succinate (1 mg/kg) for determination of plasma insulin concentration and serum concentrations of glucose, triglyceride, and NEFAs. The llamas were then fed a limited diet (grass hay, 0.25% of body weight daily) for 21 days, after which the experimental procedures were repeated. RESULTS: Compared with llamas that were not feed-restricted, llamas after feed restriction had significantly higher plasma insulin concentration and serum concentrations of triglycerides and NEFAs. Feed-restricted llamas after hydrocortisone injection had a significantly smaller increase in serum glucose concentration, a decrease (rather than an increase) in serum concentration of NEFAs, and no change in blood concentrations of insulin or triglycerides. CONCLUSIONS AND CLINICAL RELEVANCE: Short-acting glucocorticoid hormones did not appear to increase blood lipid concentrations in healthy llamas, regardless of ongoing fat mobilization. Thus, these hormones appear unlikely to be major direct contributors to diseases such as hepatic lipidosis or hyperlipemia. Although administration of hydrocortisone reduced serum concentration of fatty acids in feed-restricted llamas, its use has not been evaluated in sick camelids and cannot be considered therapeutically useful.     

Pituitary ACTH and adrenocortical secretion in critically ill dogs

OBJECTIVE: To evaluate pituitary-adrenal function in a population of critically ill dogs by measuring serial plasma concentrations of basal cortisol, ACTH-stimulated cortisol, and endogenous ACTH. DESIGN: Prospective study. ANIMALS: 20 critically ill dogs admitted to an intensive care unit (ICU). PROCEDURE: Basal plasma cortisol, ACTH-stimulated cortisol, and endogenous ACTH concentrations were measured for each dog within 24 hours of admission and daily until death, euthanasia, or discharge from the ICU. Established reference ranges for healthy dogs were used for comparison. Survival prediction index (SPI) scores were calculated for each dog within 24 hours of admission. RESULTS: No significant difference was found between initial concentrations of basal cortisol, ACTH-stimulated cortisol, and endogenous ACTH in 13 dogs that survived and those in 7 dogs that died. High initial basal endogenous ACTH concentrations were correlated with subsequent high values. Low basal ACTH-stimulated cortisol concentrations were predictive of higher subsequent values. All basal and ACTH-stimulated cortisol concentrations were within or above the reference range in the 52 plasma samples collected from the 20 dogs during hospitalization. The SPI scores correlated with outcome (ie, alive or dead), but none of the plasma hormone concentrations correlated with SPI score or outcome. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that none of the critically ill dogs in our study population developed adrenal insufficiency during hospitalization in the ICU.