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PubMed1984

Effect of angiotensin II, catecholamines and glucocorticoid on corticotropin releasing factor (CRF)-induced ACTH release in pituitary cell cultures.

The effects of angiotensin II, catecholamines and glucocorticoid on CRF-induced ACTH release were examined using rat anterior pituitary cells in monolayer culture. Synthetic ovine CRF induced a significant ACTH release in this system. Angiotensin II produced an additive effect on CRF-induced ACTH release. The ACTH releasing activity of CRF was potentiated by epinephrine and norepinephrine. Dopamine itself at 0.03-30 ng/ml did not show any significant effect on ACTH release, but it inhibited CRF-induced ACTH release. Corticosterone at 10(-7) and 10(-6)M inhibited CRF-induced ACTH release. These results indicate that angiotensin II, catecholamines and glucocorticoid modulate ACTH release at the pituitary level.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Value of assessing adrenocorticotropic hormone (ACTH) levels in differential diagnosis of hypercorticism.

Diagnosis and differential diagnosis of Cushing's syndrome remains a challenge in clinical endocrinology. The aim of this study was to establish the value of assessing adrenocorticotropic hormone (ACTH) levels in differential diagnosis of hypercorticism using receiver operating characteristic (ROC) curve. We have evaluated 114 patients with Cushing's syndrome testing the value of pathohistological examination and postoperative testing. The control group consisted of 53 obese healthy persons. ACTH level was determined using a commercial RIA (CIS, France). ACTH secreting pituitary adenoma was found in 56.14% examinees, ectopic secretion in 6.14%, cortisol secreting adrenal adenoma in 37.57%, and adrenal carcinoma in 6.14% of all patients with Cushing's syndrome. Basal ACTH level for pituitary adenoma was 107.29 +/- 75.69 pg/mL; for ectopic secretion 181.63 +/- 149.84 pg/mL; for adrenal adenoma 4.22 +/- 2.32 pg/mL; for adrenal carcinoma 5.50 +/- 7.72 pg/mL; and 34.76 = 10.07 pg/mL in control group. Testing the value of assessing ACTH the area under ROC curve was 0.9965 +/- 0.0071. Test sensitivity was 99.89% and test specificity was 97%. For ACTH cut-off level of 8 pg/mL, test sensitivity was 88.50%, with specificity of 99%. For ACTH cut-off level of 22 pg/mL, test sensitivity was 99.30%, with specificity of 98%. Our intermediate zone from 8 to 22 pg/mL confirms that assessment of ACTH level is a reliable tool in differential diagnosis of Cushing's syndrome.

Adrenocortical Hyperfunction↗
PubMed1990

Cellular responses of the rat adrenal zona fasciculata to acute ACTH stimulation: a morphometric study.

Long-term ACTH-stimulation of steroidogenesis in the rat adrenal cortex results in time-dependent increases in the surface area per cell of smooth endoplasmic reticulum and mitochondrial cristae. As the morphological responses to short-term ACTH stimulation have not been described, we undertook morphometric analyses of the effects of acute (10 min) ACTH stimulation of rat adrenocortical cells in vivo as they may be expressed in the mitochondria and the smooth endoplasmic reticulum. Six young male Wistar rats were allocated to each of four groups: 1. normal controls; 2. ACTH-treated normal rats; 3. Dexamethasone-inhibited; 4. ACTH-treated Dexamethasone-inhibited. As judged by the radio-immunoassay of trunk blood, levels of ACTH, 11-deoxycorticosterone and corticosterone were appropriate to the treatment state. ACTH activation resulted in no changes in the smooth endoplasmic reticulum; but the mitochondrial inter-membrane space was significantly increased over that of the contrasted pair. The inter-membrane space in the dexamethasone-inhibited rats was significantly less than that of all other groups. No responses to ACTH-activation were shown by the intra-cristal or matrix volumes of the mitochondria. The increased inter-membrane space appears to be caused by a decrease in the surface area of the inner mitochondrial membrane. The significance of these intra-mitochondrial changes to the rate-limiting step of steroidogenesis is discussed.

Adrenocorticotropic Hormone↗
PubMed1994

The effect of acute and chronic ACTH administration on pituitary-adrenal response to acute immobilization stress. Relationship to changes in corticosteroid-binding globulin.

The effect of single and chronic ACTH administration on serum levels of the corticosteroid-binding globulin (CBG) and pituitary-adrenal (PA) responsiveness to acute immobilization (IMO) stress was studied in adult Sprague-Dawley rats. Single ACTH administration significantly reduced CBG levels but did not alter PA response to acute IMO. Chronic ACTH administration caused a greater fall in CBG than single ACTH administration and blunted PA response to IMO. The effect of chronic ACTH administration on CGB levels recovered 2 days after the last administration, but the ACTH response to IMO was normal only by day 7 after the last ACTH injection. The present data indicate that ACTH administration to rats reduced CBG levels and impaired PA response to acute stress, but impaired PA responsiveness cannot be solely attributed to changes in CBG.

Adrenocorticotropic Hormone↗
PubMed1995

Modulatory mechanism of ACTH on insulin secretion: effect on cytosolic Ca2+, membrane potential and Ca(2+-ATPase activity.

The aim of this work was to get some insight into the mechanism by which ACTH produces its enhancing effect on glucose-induced insulin secretion. For this purpose we have determined: a) the release of insulin by isolated rat islets incubated with 3.3 or 16.6 mM glucose with or without the addition of 500 pg/ml ACTH, together with the changes induced by ACTH on b) cytosolic [Ca2+] of isolated B cells, c) islet plasma membrane Ca(2+)-ATPase activity and d) changes in membrane potential of single mouse islets. ACTH significantly enhanced the release of insulin elicited by either 3.3 or 16.6 mM glucose. This hormone concentration also induced a significant increase in the cytosolic [Ca2+] in isolated B cells. ACTH did not produce B cell membrane depolarization. Conversely, ACTH produced a significant decrease in islet plasma membrane Ca(2+)-ATPase activity. These results suggest that ACTH in concentrations similar to those attained by the endogenous peptide at the islet interstitium exerts its positive modulation on glucose-induced secretion of insulin, at least partly through its increasing effect on cytosolic [Ca2+] of B cells. The latter might be the consequence of the decreasing effect of ACTH on Ca(2+)-ATPase activity rather than to stimulation of voltage-dependent Ca(2+)-channels.

Adrenocorticotropic Hormone↗
PubMed2001

A high dose of vitamin E inhibits adrenal corticosterone synthesis in chickens treated with ACTH.

The present experiment was conducted to study the effects of dietary vitamin E on plasma corticosterone (CTC) concentration and adrenal steroid syntheses in chickens treated with adrenocorticotropic hormone (ACTH). Chickens were divided into ACTH(-) and ACTH(+) groups, and each group was further divided into three subgroups administered with vitamin E (500 or 5,000 mg/kg diet) and without the vitamin. Vitamin E (DL-alpha-tocopheryl acetate) was mixed with the basal diet at levels of 500 and 5,000 mg/kg and fed for 6 d. ACTH (20 IU/kg body weight) was given daily by intraperitoneal injection for 5 d. alpha-Tocopherol levels in the plasma and adrenal gland were markedly elevated by vitamin E feeding, and the level of adrenal free cholesterol (CHOL), which is used for steroid synthesis, was significantly decreased by vitamin E feeding in a dose-dependent manner. However, the level of adrenal CHOL ester was unchanged by any treatment. The elevations of pregnenolone, progesterone and CTC levels in the adrenal gland of chickens with ACTH treatment were decreased by vitamin E administration. The elevation of plasma CTC concentration in the ACTH(+) group was dramatically decreased by vitamin E administration, while that concentration was not influenced by the vitamin administration in the ACTH(-) group. These findings indicate that vitamin E suppresses the elevation of the plasma CTC concentration due to ACTH in chickens, possibly by inhibiting the conversion of CHOL ester to free CHOL in the adrenal gland.

Adrenal Glands↗
PubMed2006

Salivary cortisol in low dose (1 microg) ACTH test in healthy women: comparison with serum cortisol.

To date, a single report has appeared on the use of salivary cortisol for adrenal function testing with a low dose ACTH, although 1 microg has become preferred as a more physiological stimulus than the commonly used 250 microg ACTH test. Our present study was aimed to obtain physiological data on changes of free salivary cortisol after 1 microg ACTH stimulation. This approach was compared with the common method based on the changes of total serum cortisol. Intravenous, low-dose ACTH test was performed in 15 healthy women (aged 22-40 years) with normal body weight, not using hormonal contraceptives, in the follicular phase of the menstrual cycle. Blood and saliva for determination of cortisol were collected before ACTH administration and 30 and 60 min after ACTH administration. Basal concentration of salivary cortisol (mean +/- S.E.M., 15.9+/-1.96 nmol/l) increased after 1 microg ACTH to 29.1+/-2.01 nmol/l after 30 min, and to 27.4+/-2.15 nmol/l after 60 min. The differences between basal and stimulated values were highly significant (p<0.0001). The values of salivary cortisol displayed very little interindividual variability (p<0.04) in contrast to total serum cortisol values (p<0.0001) A comparison of areas under the curve (AUC) related to initial values indicated significantly higher AUC values for salivary cortisol than for total serum cortisol (1.89+/-0.88 vs. 1.22+/-0.19, p<0.01). Correlation analysis of serum and salivary cortisol levels showed a borderline relationship between basal levels (r=0.5183, p=0.0525); correlations after stimulation were not significant. Low-dose ACTH administration appeared as a sufficient stimulus for increasing salivary cortisol to a range considered as a normal adrenal functional reserve.

Adrenal Glands↗
PubMed1992

[Effects of ANF and ACTH on aldosterone secretion in cultured human adrenal tissue].

We studied the effects of various concentrations of ANF and ACTH on aldosterone secretion in human normal adrenal tissue over different response times in vitro. We found that ANF 10(-8) mol/L at first stimulated but 24 h later inhibited basal aldosterone secretion. ANF 10(-8) mol/L also inhibited the ACTH-stimulated secretion of aldosterone. ACTH 10(-8) mol/L did not stimulate aldosterone secretion, while ACTH concentrations of 3 x 10(-8) and 5 x 10(-8) mol/L did. When ACTH and ANF were added simultaneously, the ANF-induced inhibition of ACTH-stimulated aldosterone secretion could be overcome by increasing the concentration of ACTH. Our results show that ANF caused a dose-dependent and time-dependent inhibition of basal and ACTH-stimulated increases in aldosterone secretion.

Adrenal Glands↗
PubMed2006

[Influence of ACTH-depot doses on neuroendocrine gestosis treatment].

OBJECTIVE OF THE STUDY: Two dosing methods of ACTH-depot therapy were compared dependently on gestational age and sequence of applied injections. It has been concluded that better efficacy was observed in single doses method comparing to serial doses in 2nd trimester. MATERIAL AND METHODS: Retrospectively, 380 pregnancies were analyzed, in which ACTH-depot therapy was applied using 0,5 mg doses. In 140 subjects (Group I, 1990-1991) 3 injection series every 2nd day with additional antibiotic (i.e. Monural 3g) were administrated. In the rest 240 (Group II, 1997-2002) single doses were applied during the whole period of pregnancy due to recurrent vomiting or decreased CAP1 serum levels under 0,8 micromol/l/min and CAP2 under 1,4 micromol/l/min in 1st trimester and compulsory in ACTH serum levels under 5,0 pg/ml. RESULTS: Clinical results can be compared with oxytocinase and ACTH serum levels, what allows to understand enzymatic control of internal maternal state. Role of ACTH not only in lung maturation, but also in onset of labor was proved in the mechanism of influence on immunologic tolerance. In hormonal threatening pregnancies enzymatic component is less helpful in predicting birth date because of common irregular oxitocinase pattern in such patients. On the other hand constant enzymatic increase proves effectiveness of ACTH-depot therapy in neurendocrine-gestoses, or in insulin-requiring pregnant patients. CONCLUSIONS: Acquired results of neonatal state proved that: 1. in pregnancies after infertility treatment early application of substitutional hormonotherapy wsith single doses of 0,5 mg ACTH-depot in early gestational weeks is more efficient method of ACTH dosing than 3 injections method in 2nd trimester 2. serum prelabour oxitocinase levels were precise factors of clinical results.

Adrenal Insufficiency↗
PubMed1990

Adrenocorticotropin (ACTH) functions as a late-acting B cell growth factor and synergizes with interleukin 5.

In recent years there has been considerable discussion of possible cross-regulatory mechanisms involving the immune system and the neuroendocrine system. Certainly, evidence of hormonal communication between these two systems would provide at least a partial explanation for the many anecdotal observations of physical and mental stress affecting disease course. In previous studies of a neoplastic lymphokine-responsive B cell clone, BCL1-3B3, we noted that these cells produced a lymphokine which could affect normal B cell growth and viability. Physical characterization of this lymphokine indicated that its molecular weight was identical to that of the neuroendocrine hormone adrenocorticotropin (ACTH). Since Blalock and colleagues had reported the production of ACTH by virally-infected B cells, we have investigated whether ACTH can functionally mimic the BCL1-3B3-derived lymphokine. The neuroendocrine hormone adrenocorticotropin (ACTH) can increase in vitro murine B lymphocyte proliferation when added at physiologically relevant concentrations between 10(-9) to 10(-11) M. ACTH does not mimic the action of any lymphokine known to be required for B cell proliferation such as IL-2, IL-4, or IL-5. ACTH requires the presence of one or more of these known B cell stimulatory factors for its action and the most marked increase in B cell proliferation were noted in assays for IL-5 activity where 10(-10) M ACTH increased thymidine incorporation up to five-fold. Using two-stage assays, we determined that ACTH acts during the latter stages of B cell activation (i.e., 3-4 days after initial stimulation with either the combination of IL-4, GAMIg-Sepharose, and IL-1 or the combination of DxS and IL-5). These data indicate a direct role for a stress-induced neuroendocrine hormone in modulating the course of a humoral immune response.

Adrenocorticotropic Hormone↗
PubMed1978

Role of cyclic AMP and protein kinase on the steroidogenic action of ACTH, prostaglandin E1 and dibutyryl cyclic AMP in normal adrenal cells and adrenal tumor cells from humans.

The role of the cyclic AMP-protein kinase system in mediating the steroidogenic effect of ACTH, prostaglandin E1 and dibutyryl cyclic AMP, induced similar stimulations of protein kinase activity, cyclic AMP was studied using human adrenal cells isolated from normal and adrenocortical secreting tumors. At high concentrations of ACTH, complete activation of protein kinase of normal adrenal cells was observed within 3 min, at the time when cyclic AMP production was slightly increased and there was still no stimulation of steroidogenesis. At supramaximal concentrations, ACTH, PGE1 and dibutyryl cyclic AMP and cortisol productions in adrenal cells isolated from normal and from one adrenocortical tumor. In one tumor in which the adenylate cyclase activity was insensitive to ACTH, the hormone was unable to stimulate protein kinase or steroidogenesis, but the cells responded to both PGE1 and dibutyryl cyclic AMP. In another tumor in which the adenylate cyclase was insensitive to PGE1, this compound also did not increase protein kinase activity or steroidogenesis, but both parameters were stimulated by ACTH and dibutyryl cyclic AMP. After incubation of normal adrenal cells with increasing concentrations of ACTH (0.01-100 nM) marked differences were found between cyclic AMP formation and cortisol production. However at the lowest concentrations of ACTH exerting an effect on steroid production a close linked correlation was found between protein kinase activation and cortisol production, but half-maximal and maximal cortisol production occurs at lower concentration of ACTH than was necessary to induce the same stimulation of protein kinase. Similar findings were found after incubating the adrenal cells with dibutyryl cyclic AMP (0.01-10 mM). The results implicate an important role of the cyclic AMP-protein kinase system during activation of adrenal cell steroidogenesis by low concentrations of steroidogenic compounds.

Adenylyl Cyclases↗
PubMed1990

Role of the fourth cerebroventricle in mediating rat plasma ACTH responses to intravenous nicotine.

Peripherally administered nicotine elevates rat plasma adrenocorticotropic hormone (ACTH) levels, acting at brain regions adjacent to or downstream from the third cerebroventricle. Studies evaluated whether the paraventricular nucleus (PVN) mediates directly the ACTH response to nicotine administered i.v. and if regions adjacent to the fourth ventricle (IV) are involved. Direct involvement of the PVN in the release of ACTH in response to i.v. nicotine (0.03 or 0.01 mg/kg b.wt.) was refuted by studies in which the administration of the nicotinic cholinergic antagonist, mecamylamine (20 or 40 micrograms bilaterally adjacent to the PVN), failed to block ACTH secretion. To activate sites distal to the third ventricle, nicotine (0.25, 0.5, 2.5 or 5.0 micrograms) was injected into the IV; ACTH levels peaked between 3 and 7 min. Nicotine 0.25 micrograms injected into the IV elevated ACTH to levels within the range of those produced by i.v. nicotine (0.03 mg/kg b.wt.). To confirm that sites accessible from the IV are involved, mecamylamine was administered i.v. (0.5 or 1.0 mg/kg b.wt.) or into the IV (4 or 40 micrograms) and nicotine was delivered by the opposite route. Intravenous mecamylamine reduced the plasma ACTH response to 0.25 micrograms of nicotine in the IV. Mecamylamine, administered into the IV before i.v. nicotine (0.03 mg/kg b.wt.) antagonized the effect of nicotine. These results indicate that stimulation of ACTH secretion by nicotine delivered i.v. occurs via structures accessible from the IV. In contrast to prevailing ideas, the PVN does not appear to be the direct site of action of nicotine.

Adrenocorticotropic Hormone↗
PubMed1989

The effect of magnesium valproate on plasma ACTH concentrations in Nelson's syndrome.

Sodium valproate, a gamma-aminobutyric acid (GABA) agonist, was found to decrease plasma ACTH concentration in some cases of Cushing's disease and Nelson's syndrome. In this study we have investigated the influence of magnesium valproate (MV), a newly introduced salt of valproic acid, on plasma ACTH levels in 8 patients with Nelson's syndrome. The daily dose, 1200 mg of MV, significantly decreased plasma ACTH level at 10 p.m. compared with placebo. A single dose of 400 mg of MV, led to a reduction in plasma ACTH concentration only in two out of seven patients during a four-hour observation. The fall in plasma ACTH level in the same patients at 10 p.m., after the next two doses of this drug, suggests that single dose may be insufficient for introducing GABA-dependent reduction in ACTH release. During a long-term therapy with MV, in all three patients investigated a marked decrease in plasma ACTH was observed. Our results suggest that magnesium valproate may be useful during chronic therapy in some patients with ACTH hypersecretion.

Adrenocorticotropic Hormone↗
PubMed1985

Effect of exogenous ACTH on serum corticosterone and cortisol concentrations in the Moluccan cockatoo (Cacatua moluccensis).

The effects of exogenous adrenocorticortrophic hormone (ACTH) on the serum corticosterone and cortisol concentrations were determined in 28 mature Moluccan cockatoos (Cacatua moluccensis), a representative of the psittacine species. Birds were randomly assigned to 4 groups (2 ACTH-treated groups and 2 saline-treated controls). Group I (10 cockatoos [5 males and 5 females] ) was given 15 IU of ACTH after blood samples (base line) were taken at 10:00 AM. Blood samples were taken again at 30 minutes and 2.5 hours after ACTH administration. Group II (10 cockatoos) was given similar treatment, but blood samples were taken at 1 and 4 hours after ACTH was administered. Groups III and IV (each of 4 birds) were given saline solution injections as controls. Blood samples were taken at 30 minutes and 2.5 hours after injection (group III) and at 1 and 4 hours after injection (group IV). All serum samples were analyzed for cortisol and corticosterone. Serum corticosterone concentration increased significantly (P less than 0.01) from base-line levels (26 ng/ml) to 108 ng/ml within 30 minutes after ACTH was administered. The high values were maintained for 3 hours and then decreased to 40 ng/ml at the end of 4 hours. Male birds seemed to respond to the ACTH treatment quickly and maintained increased concentration for a shorter period when compared with the responses seen in female birds. Serum cortisol values remained low throughout the experimental period. These results indicate that serum corticosterone was responsive to ACTH administration, but cortisol was not. In addition, there may be a difference in the responses between male and female members of the species.

Adrenal Glands↗
PubMed1986

Inhibition of ACTH action on cultured bovine adrenal cortical cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin through a redistribution of cholesterol.

The conversion of cholesterol to cortisol by cultured bovine adrenal cortical cells is stimulated 6-fold by adrenocorticotropin and is limited by the movement of cholesterol to the mitochondria (DiBartolomeis, M.J., and Jefcoate, C.R. (1984) J. Biol. Chem. 259, 10159-10167). Exposure of confluent cultures to the potent environmental toxicant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (10(-8)M), for 24 h prior to adrenocorticotropin (ACTH) addition decreased the rate of ACTH-stimulated steroidogenesis but did not affect the basal rate. TCDD was more effective against stimulation at 10(-11) M ACTH (4-fold) than at 10(-7) M ACTH (10%), consistent with an increase in EC50 for ACTH. Stimulation of bovine adrenal cortical cells by cAMP was similarly decreased by TCDD. In both cases the effectiveness of TCDD increased with time of exposure to the stimulant. The transfer of cholesterol to mitochondria in intact cells was quantitated by means of the 2-h accumulation of mitochondrial cholesterol in the presence of aminoglutethimide, an inhibitor of cholesterol side chain cleavage. Although cholesterol accumulated in the presence of ACTH (13 to 28 micrograms/mg), pretreatment of cells with TCDD caused a decrease in mitochondrial cholesterol (13 to 8 micrograms/mg). The effect of TCDD was produced relatively rapidly (t1/2 approximately 4 h). In absence of TCDD, the mitochondria of ACTH-stimulated cells also eventually lose cholesterol (after 2 h). It is concluded that TCDD pretreatment may increase the presence of a protein(s) that cause mitochondrial cholesterol depletion when the cells are stimulated by ACTH or cAMP. TCDD-enhanced cholesterol efflux from mitochondria diminishes cholesterol side chain cleavage when mitochondrial cholesterol is sufficiently depleted (after 2-4 h).

Adrenal Cortex↗
PubMed1984

In vitro responses of aldosterone-producing adenomas to angiotensin II and ACTH after treatment with spironolactone before adrenalectomy.

Aldosterone-producing adenomas in patients who have not been given spironolactone are more responsive to ACTH than to angiotensin II. In vitro, adenomas respond to ACTH, but their response to angiotensin II has not been clearly defined. Treatment with spironolactone has been given before the removal of some of the adenomas studied in vitro, and it can blunt increases in plasma aldosterone concentrations that occur in response to increases in renin activity. To assess the effect of preoperative spironolactone therapy on the responsiveness of aldosterone-producing adenomas in vitro, tissue from five patients with adenomas was incubated for 4 hours with and without angiotensin II and ACTH, 10(-7) to 10(-5) mol/L. The responsiveness of the adenomas was then related to the duration of preoperative spironolactone therapy. The serum potassium concentration was normal in the patients before the operations. Adenoma tissue from a patient given spironolactone for 4 days was responsive to angiotensin II and to ACTH. Treatment of longer duration with spironolactone appeared to be associated with a pattern of decreasing responsiveness to ACTH and an absence of response to angiotensin II in vitro. Aldosterone production by nonadenomatous adrenal tissue did not respond to angiotensin II or to ACTH. Our results suggest that preoperative spironolactone therapy might decrease the responsiveness of aldosterone-producing adenomas to angiotensin II and ACTH in vitro. Therefore, studies of aldosterone-producing adenomas in vitro should consider the possible effects of preoperative treatment with spironolactone on the responsiveness of the adenomas to angiotensin II and ACTH.

Adenoma↗
PubMed1995

[Adrenocorticotropic hormone (ACTH): antagonistic effect on opioid analgesia in central nervous system of the rat and its possible mechanisms of action].

Using the behavioral pharmacological approach, we have studied the influence of ACTH on the analgesia mediated by three types of opioid receptors (mu, delta, kappa). The mechanisms by which ACTH antagonizes opioid analgesia were explored at receptor level and post-receptor second messenger level. The expression of Fos protein induced by ACTH was also observed in rat brain. The main results show that ACTH selectively antagonizes spinal opioid analgesia mediated by mu and delta, but not kappa receptors. The proposed mechanisms of the anti-opioid effect of ACTH are that ACTH can modulate opioid-induced decrease of intracellular cAMP content and the suppression of calcium influx. ACTH has been shown to induce Fos protein expression in selected brain areas including the nuclei involved in pain modulation. These brain areas may serve as sites of action for ACTH to exert its anti-opioid effect.

Analgesics, Non-Narcotic↗
PubMed1995

[Hypothalamic-adenohypophysial function of corticotropin releasing hormone (CRH)-ACTH system in brain death].

To evaluate the hypothalamic-adenohypophysial function of corticotropin releasing hormone (CRH)-ACTH system in brain death, basal serum values of ACTH and cortisol was measured, and in addition, insulin-tolerance test (ITT) and CRH stimulation test was performed is 28 brain death cases. Basal levels of ACTH were low-normal, whereas those of cortisol were high-normal, and no correlation was observed between them. There was no correlation between these levels and the age, sex, cause of the brain death, and the incidence of hypotention. However, basal ACTH value significantly decreased within a few days (p < 0.01), and ACTH was undetectable in all cases 5 days after the diagnosis of the brain death. On the other hand, ITT and CRH test was negative in all cases. These results suggest that some degree of adenohypophysial function of ACTH secretion remains for a few days after the diagnosis of the brain death. Compared with other adenohypophysial hormones of the brain death cases in previous reports, however, ACTH was lower, decreased more rapidly, and did not response to the direct pituitary stimulation test, the CRH test. These results further suggest that disturbance of ACTH secretion occurs from an early stage in the brain death cases.

Adolescent↗