The Effect of Adrenocorticotropic Hormone in Panhypopituitarism 1

Bartter, Frederic C.; Fourman, Paul; Albright, Fuller; Forbes, Alexander; Jefferies, William McK.; Griswold, Grace C.; Dempsey, Eleanor; Bryant, Dorothy; Carroll, Evelyn L.

doi:10.1172/jci102330

Cited by 62 publications

(12 citation statements)

References 5 publications

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“…In most respects, the effects produced by ACTH under the condition of this experiment resemble those previously described in non-diabetic individuals (2)(3)(4)(5)(6)(7)(8). Net losses of nitrogen, excess potassium, phosphorus, and calcium resulted from administration of the hormone and the glomerular filtration rate, as estimated from the endogenous creatinine clearance, was increased.…”

Section: Methodssupporting

confidence: 75%

Studies Concerning the Role of the Adrenal Cortex in the Pathologic Physiology of Diabetic Acidosis. II. The Identification of Adrenal-Conditioned Factors in the Physiologic Reaction to the Stress of Insulin Deprivation1

McArthur¹,

Gautier²,

Swallow³

et al. 1954

J. Clin. Invest.

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In a descriptive study designed to correlate changes in the level of adrenal cortical function with other metabolic phenomena occurring during the evolution of experimental diabetic acidosis it was observed (1) that eosinopenia and an increase in the rate of corticosteroid excretion are comparatively late features of ketoacidosis induced by the omission of insulin. A close temporal relation was found to obtain between evidences of increased adrenal activity and the following metabolic events: (a) An acceleration in the rate of catabolism of protoplasm; (b) a loss of potassium in excess of nitrogen; and (c) a decreased sensitivity to injected insulin. In some, but not all, experiments it appeared that adrenal activation was related in time to the occurrence of increased lipemia and ketonemia as well.In this paper are presented the results of experiments designed to ascertain whether the above events, temporally linked to increased adrenal activity, can, in fact, be regarded as adrenal conditioned. The postulates underlying these experiments are that metabolic reactions dependent upon increased adrenal activity for their initiation or maintenance should be susceptible to: (a) Premature induction by exogenous stimulation of the adrenal cortex during mild stress; and (b) diminution or suppression by maintenance of a fixed Accordingly, the experiments comprise a comparison between the metabolic changes which characterize the stressful terminal phases of insulin deprivation in the depancreatized dog and: (a) The changes which accompany the induction of a comparable degree of eosinopenia by the administration of ACTH to a depancreatized dog deprived of insulin for a relatively brief period; and (b) the changes which accompany the withdrawal of insulin from an adrenalectomized-depancreatized animal maintained upon a fixed dose of adrenal cortical hormones. EXPERIMENTAL PROCEDUREResponse of the depancreatized dog to exogenous stimulation of the adrenal cortex. A balance study was performed upon an animal (Frisky) whose metabolic response to insulin deprivation had been well established by previous withdrawal experiments (1). After being stabilized on the same diet as had been employed for previous balance studies, the From the results of previous experiments it was known to restore the pre-adrenalectomy insulin requirement. that a loss of excess potassium, presumably associated The maintenance regime upon which the animal was ultiwith hepatic glycogenolysis, would occur during the mately stabilized comprised: (a) 12-hourly feedings confirst 12 hours and that the losses of nitrogen and potas-taining 30 mEq. of sodium and 65 mEq. each of potassium sium would be in protoplasmic proportion during the and chloride, and (b) 12-hourly administration of 25 to succeeding 24 hours. 30 units of crystalline insulin subcutaneously, and of 2.25 Response of the adrenalectomized-depancreatised dog to mg. of desoxycorticosterone acetate and 10 mg. of cortiinsulin deprivation. A balance study was performed upon sone acetate intramuscula...

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Section: Methodssupporting

confidence: 75%

Studies Concerning the Role of the Adrenal Cortex in the Pathologic Physiology of Diabetic Acidosis. II. The Identification of Adrenal-Conditioned Factors in the Physiologic Reaction to the Stress of Insulin Deprivation1

McArthur¹,

Gautier²,

Swallow³

et al. 1954

J. Clin. Invest.

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“…(Figure 1). As discussed elsewhere (7,16) this effect may be due to the pitressin present in the ACTH as a contaminant (Table I). Comparison of the actual weight curves with the "theoretical" weight curves based on N-plus-K-plus Na (Figures 3, 6, and 9) shows that water was retained without electrolytes during ACTH therapy-presumably a pitressin effect-in the experiments on T. McH.…”

Section: C) Calcium Metabolismmentioning

confidence: 83%

“…Since the effect of adrenocorticotropic hormone (ACTH) in subjects with normal adrenals is essentially to produce a temporary "Cushing's syndrome medicamentosa" (3)(4)(5)(6)(7) it was of interest to observe the effects of ACTH in the adrenogenital syndrome. The first part of this report concerns the effects of ACTH in three female patients with the adrenogenital syndrome.…”

mentioning

confidence: 99%

The Effects of Adrenocorticotropic Hormone and Cortisone in the Adrenogenital Syndrome Associated With Congenital Adrenal Hyperplasia: An Attempt to Explain and Correct Its Disordered Hormonal Pattern 12

Bartter¹,

Albright²,

Forbes³

et al. 1951

J. Clin. Invest.

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169

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“…2) A transfer of potassium from muscle to liver glycogen may have occurred, as 12 Calculated using muscle analyses (Table II), and assuming that the muscle mass is 41% of body weight (11), and that other tissues were not significantly depleted. suggested by Bartter and associates from observations on patients receiving adrenocorticotropic hormone (9).…”

mentioning

confidence: 99%

“…A repeat biopsy from the pectoral muscle was performed on the 11th postoperative day. Tissue water and electrolyte distributions (Table II) (9), except that in case 1 the ratios, K/N = 2.9 and P/N = .054, were derived from the patient's first muscle biopsy (Table II); and in case 2, the ratios, K/N = 2.8 and P/N = .064, were derived from the means of muscle analyses in five chronically ill hospital patients who had no evidence of electrolyte disturbance (4). In computing intracellular balances, corrections for insensible skin losses were made by subtracting algebraically the average of the control period balances from the found balance values.…”

mentioning

confidence: 99%

Postoperative Potassium Deficit and Metabolic Alkalosis. The Pathogenic Significance of Operative Trauma and of Potassium and Phosphorus Deprivation 1

Eliel¹,

Pearson²,

White³

1952

J. Clin. Invest.

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Patients maintained postoperatively on parenteral fluids or a dietary intake low or lacking in potassium may develop a syndrome characterized by apathy, lethargy, muscular weakness, abdominal distension and ileus, cardiac arrhythmias and edema; and occasionally by confusion, delirium, muscular twitching and tetany. A clinical description of the syndrome as observed in 32 postoperative patients has appeared elsewhere (1). Evidence was found in these patients for the existence of potassium deficit, namely: 1) the presence of hypopotassemia, hypochloremia and metabolic alkalosis, 2) electrocardiographic changes consistent with potassium deficit, 3) extensive expansion of the radiosodium space beyond the confines of the bromide space, suggesting that sodium had migrated into the cells to replace lost potassium, 4) lowering of erythrocyte potassium and increase of erythrocyte sodium concentrations in several patients, and 5) prompt reversal of the clinical and blood chemical abnormalities upon administration of adequate amounts of potassium.Two factors were thought to be of primary importance in the pathogenesis of the potassium deficit in the group studied: 1) adrenal cortical hyperfunction resulting from trauma ("alarm reaction") and leading to increased renal excretion of potassium and 2) a low potassium intake with poor renal conservation of potassium. was suggested by the fact that muscular weakness, hypopotassemia, hypochloremia, and metabolic alkalosis are often observed in patients with Cushing's syndrome or in patients receiving ACTH (adrenocorticotropic hormone) or cortisone (1, 2); the second by the fact that all the postoperative patients but one were on a low potassium intake when the syndrome developed. The two studies described in this paper were undertaken to evaluate the relative roles of low potassium intake and operative trauma in the production of the syndrome. Adrenal cortical hyperfunction, as estimated by several criteria, developed following the operative trauma in each case but was not separately evaluated in these studies. Hyperadrenocortical states have been induced in patients with neoplastic and other diseases by administration of adrenocorticotropic hormone (ACTH) or cortisone (1l-dehydro-17-hydroxycorticosterone); and the resulting metabolic effects have been reported in detail (24).The first study (case 1, N. M.) was designed to reproduce approximately the conditions under which the syndrome had been observed to develop, namely, simultaneous deprivation at the time of operation of potassium and phosphorus. These elements were later restored one at a time. In the second study (case 2, M. B.) a period of potassium and phosphorus deprivation was imposed preoperatively, while the operation was performed during a period when these elements were provided in adequate amounts. Both patients underwent major surgery for suspected or proved neoplasms.5 6 We are indebted to Dr. Gordon McNeer and the Gastric and Mixed Tumor Service of Memorial Center, for the opportunity to study these patients. LE...

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The Effect of Adrenocorticotropic Hormone in Panhypopituitarism 1

Cited by 62 publications

References 5 publications

Studies Concerning the Role of the Adrenal Cortex in the Pathologic Physiology of Diabetic Acidosis. II. The Identification of Adrenal-Conditioned Factors in the Physiologic Reaction to the Stress of Insulin Deprivation1

Studies Concerning the Role of the Adrenal Cortex in the Pathologic Physiology of Diabetic Acidosis. II. The Identification of Adrenal-Conditioned Factors in the Physiologic Reaction to the Stress of Insulin Deprivation1

The Effects of Adrenocorticotropic Hormone and Cortisone in the Adrenogenital Syndrome Associated With Congenital Adrenal Hyperplasia: An Attempt to Explain and Correct Its Disordered Hormonal Pattern 12

Postoperative Potassium Deficit and Metabolic Alkalosis. The Pathogenic Significance of Operative Trauma and of Potassium and Phosphorus Deprivation 1

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