A comparison of the NAHD reaction with lipoid stains in the adrenal cortex of the rat.
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Disturbed adrenal function may present in various ways. Here are outlined some of the functions of the adrenals and the clinical effects of adrenal disorder, followed by a more detailed consideration of the application of laboratory tests to the identification of adrenocortical hypo- and hyperfunction.
Effects of thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH) on plasma concentrations of thyroid hormones, and effects of ACTH and dexamethasone on plasma concentrations of cortisol, were studied in adult male ferrets. Thirteen ferrets were randomly assigned to test or control groups of eight and five animals, respectively. Combined (test + control groups) mean basal plasma thyroxine (T4) values were different between the TRH (1.81 +/- 0.41 micrograms/dl, mean +/- SD) and TSH (2.69 +/- 0.87 micrograms/dl) experiments, which were performed 2 months apart. Plasma T4 values significantly (P less than 0.05) increased as early as 2 hours (3.37 +/- 1.10 micrograms/dl) and remained high until 6 hours (3.45 +/- 0.86 micrograms/dl) after IV injection of 1 IU of TSH/ferret. In contrast, IV injection of 500 micrograms of TRH/ferret did not induce a significant increase until 6 hours (2.75 +/- 0.79) after injection, and induced side effects of hyperventilation, salivation, vomiting, and sedation. There was no significant increase in triiodothyronine (T3) values following TSH or TRH administration. Combined mean basal plasma cortisol values were not significantly different between ACTH stimulation (1.29 +/- 0.84 micrograms/dl) and dexamethasone suppression test (0.74 +/- 0.56 micrograms/dl) experiments. Intravenous injection of 0.5 IU of ACTH/ferret induced a significant increase in plasma cortisol concentrations by 30 minutes (5.26 +/- 1.21 micrograms/dl), which persisted until 60 minutes (5.17 +/- 1.99 micrograms/dl) after injection. Plasma cortisol values significantly decreased as early as 1 hour (0.41 +/- 0.13 micrograms/dl), and had further decreased by 5 hours (0.26 +/- 0.15 micrograms/dl) following IV injection of 0.2 mg of dexamethasone/ferret.(ABSTRACT TRUNCATED AT 250 WORDS)
During the dexamethasone suppression test (DST), we evaluated the relationship between the 8 a.m. dexamethasone (DXM) level and the pharmacokinetics of this corticoid after the oral administration of a single dose at midnight of DXM (1 mg) in 7 healthy subjects. The half-life time of the terminal phase for DXM was 283 min +/- 132 min (mean +/- s.d.). The 8 a.m. DXM level, which is positively correlated with the DXM half-life time, is useful for the interpretation of the DST. On the other hand, no correlation was observed between the 8 a.m. plasma cortisol and DXM levels in 21 healthy subjects. However, the negative correlation between the dose of DXM/kg and post-DXM cortisol level suggests the possibility of adjusting the dose of DXM in obese patients.
The utility of a low dose (1 microgram/kg) synthetic ACTH challenge test in detecting moderate reductions in adrenocortical sensitivity in dogs was examined. First, the adrenocortical responses to an intravenous bolus of either 1 microgram/kg or 0.25 mg per dog of synthetic ACTH were compared in two groups of normal dogs. While plasma cortisol concentrations were similar in both groups 60 minutes after ACTH injection, dogs given 0.25 mg ACTH showed continued elevations in plasma cortisol concentrations at 90 and 120 minutes after ACTH injection. Later, the dogs previously tested with the 1 microgram/kg ACTH challenge were given a single intramuscular dose of prednisone (2.2 mg/kg) and retested with 1 microgram/kg of ACTH one week later. Plasma cortisol levels were significantly reduced after ACTH injection in dogs previously given prednisone demonstrating that a single intramuscular prednisone dose causes detectable adrenocortical suppression one week after administration. The 1 microgram/kg synthetic ACTH challenge test provides a sensitive means for evaluating adrenocortical suppression in dogs.
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The adrenocortical response to the simple 30-minute ACTH stimulation test was compared with the hypothalamic-pituitary-adrenocortical (HPA) response to insulin-induced hypoglycaemia in 25 patients with various degrees of hypothalamic-pituitary malfunction. The correlations between the increase in plasma cortisol during insulin hypoglycaemia and that during ACTH stimulation (r = 0-66) and between peak plasma cortisol levels during the two tests (r = 0-90) were highly significant. Peak plasma cortisol levels in individual patients were similar on both tests, no patient showing any major discrepancy between the two test results. Thus the simple 30-minute ACTH stimulation test seems to be reliable in detecting imparied HPA function.
Adrenocortical function, as reflected by sequential analysis of plasma cortisol and adrenocorticotropin (ACTH) test, was investigated in elderly patients (greater than or equal to 65 years) with acute myocardial infarction (AMI), and compared to young patients (less than or equal to 55 years) with AMI. Further, age-matched subjects admitted with ischaemic chest pain, in whom AMI was not verified, served as controls. Following infarction, plasma cortisol peaked within 24 hours in both age groups, whereupon the cortisol level gradually decreased till day 12. Plasma cortisol during AMI disclosed no age-related difference, but was significantly correlated to the localization of infarction and lactate dehydrogenase (LDH). The development of complications, i.e. hypotension, congestive heart failure, and arrhythmia, calling for therapeutic intervention, was solely correlated to infarct size, as estimated by peak LDH. Young and elderly patients responded equally and normally to ACTH stimulation, and in both groups a significant, positive correlation between the basal and the 30-min plasma cortisol was observed. Thus, we may conclude that in patients with AMI, the hypothalamic-pituitary-adrenocortical (HPA) response to stress and ACTH test shows no repression due to age.