Changes in Patterns of Secretion of Corticosteroids in Rabbits after Prolonged Treatment with ACTH.

Kass, Edward H.; Hechteb, O.; Macchi, I. A.; Mou, Thomas W.

doi:10.3181/00379727-85-20959

Cited by 76 publications

(31 citation statements)

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“…An example of such a change may perhaps be found in the observation of Kass, Hechter, Macchi and Mou that prolonged ACTH administration altered the ratio of hydrocortisone to corticosterone in the adrenal vein blood of rabbits (41). A possible relationship between the corticotropin-stimulated adrenal cortex and naturally-occurring adrenal cortical hyperplasia remains a subject for future investigation.…”

mentioning

confidence: 99%

Studies in Cushing's Syndrome. Iii. Urinary 17-Ketosteroids in Patients With Bilateral Adrenal Cortical Hyperplasia*

Jailer¹,

Wiele²,

Christy³

et al. 1959

J. Clin. Invest.

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mentioning

confidence: 99%

Studies in Cushing's Syndrome. Iii. Urinary 17-Ketosteroids in Patients With Bilateral Adrenal Cortical Hyperplasia*

Jailer¹,

Wiele²,

Christy³

et al. 1959

J. Clin. Invest.

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“…In their study of peripheral blood of individuals given ACTH, the ratio of F to a compound tentatively identified as B was > 4 and for untreated individuals was > 5. However, the calculated ratio is somewhat less than the F to B ratio of 11 for material isolated from adrenal vein blood by Romanoff, Hudson, and Pincus (15) (25) of an increasing ratio of F to B in the peripheral blood of rabbits which were injected with ACTH up to periods of four weeks. In addition, Bush (26) has found a plasma F to "B" ratio of 20 to 1 in adrenal vein blood of a patient with Cushing's syndrome; a figure that compares quite well with the calculated production ratios of these compounds in our three patients with Cushing's syndrome.…”

mentioning

confidence: 67%

“…than that found after the infusion of ACTH ( Figure 1); and greater in the other two subjects with Cushing's syndrome than that found in normal individuals not given ACTH. However, the proportion of alpha-ketols present ( Figure 2 and (25). They demonstrated an increase of compound F and a progressive decrease in compound B in the adrenal vein blood of rabbits measured at the 7th, and the 21st to 28th day of ACTH injection.…”

Section: Commentmentioning

confidence: 99%

The Effect of Acth and Pathological Increases in Adrenal Cortical Function on Urinary Alphaketolic Steroid Metabolites 1

Dohan¹,

Touchstone²,

Richardson³

et al. 1955

J. Clin. Invest.

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Previous studies ( 1 ) have shown that the specific alpha-ketolic steroid metabolites found in the urine after administration of a known alphaketolic steroid reflect, to a limited extent, the nature of the precursor. With this study as a baseline, we have determined the major urinary alphaketolic steroid metabolites found after intravenous infusion of human subjects with ACTH, and some of those found in the urine of a man with Cushing's syndrome, and in that of a woman with metastatic adrenocortical carcinoma. The results of this study and some speculations concerning the possible nature and rate of alpha-ketolic steroid secretion are presented in this paper. METHODS

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“…This seems to be characteristic of the adrenal secretion of various animals tested by present day methods (10,(13)(14)(15). However, with only an occasional exception, the range of values was generally similar in all three groups of animals.…”

Section: Methodsmentioning

confidence: 88%

The Effect of Potassium Deficiency Upon Adrenocortical Secretion in the Rat 1

Rosenman¹,

George²,

Freed³

et al. 1955

J. Clin. Invest.

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The potassium-deficient rat exhibits several features in common with the untreated adrenalectomized rat, among which are subnormal growth. lowered blood pressure (1-3), diminished blood pressure responsiveness to pressor substances (4), and decreased tolerance to trauma. It therefore was considered important to determine whether the depressor response induced by potassium depletion might in fact be due to an associated state of adrenocortical insufficiency induced by the chronic potassium depletion. Such a mechanism appeared plausible particularly in view of our finding that the administration of cortisone rapidly returns the lowered blood pressures induced by potassium deficiency in rats to their initially normotensive (5) or hypertensive levels (6). MATERIALS AND METHODSA series of male rats (Long-Evans strain), initially aged 5 to 6 weeks, was used in this investigation. The rats were divided into three groups. One group of 6 rats (I) was fed a synthetic ration deficient in potassium, as previously described (2) 2As determined by flame photometry of ashed diet. left kidney was "slipped" out of its capsule and removed after ligation of its vascular pedicle. A polyethylene cannula was introduced into the left renal vein through a small incision just proximal to the pedicle ligature and was ligated in place in such a manner that its bevelled distal tip approximated the left adrenal vein as the latter entered into the renal vein. Any accessory veins which emptied into the adrenal vein were then ligated. Another ligature was placed about the left renal vein at the juncture with the inferior vena cava. The cannula was brought out through a left lateral stab wound, the abdominal incision closed and the animal placed in a restraining cage. The adrenal venous blood was drained by gravity into a cold, heparinized test tube held in a chilled container filled with ice. In general, collection of blood was continued over a period of 60 to 120 minutes, during which 2.5 to 4.0 ml. of blood was obtained.Each sample of adrenal venous blood was subjected to the following analysis for its steroid content. One to 2 ml. of plasma were extracted with 50 ml. of chloroform. The phenylhydrazine chromogen was extracted with 1 ml. reagent and developed overnight at room temperature according to the procedure of Silber and Porter (8). The curves of the reactive steroids were read between 320 and 450 muA, using 0.5 ml. cuvettes in a Beckman Model DU spectrophotometer. From these data values were computed for steroids absorbing maximally at 350 and 410 msu, by the system of Vickerstaff (9)

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Changes in Patterns of Secretion of Corticosteroids in Rabbits after Prolonged Treatment with ACTH.

Cited by 76 publications

References 0 publications

Studies in Cushing's Syndrome. Iii. Urinary 17-Ketosteroids in Patients With Bilateral Adrenal Cortical Hyperplasia*

Studies in Cushing's Syndrome. Iii. Urinary 17-Ketosteroids in Patients With Bilateral Adrenal Cortical Hyperplasia*

The Effect of Acth and Pathological Increases in Adrenal Cortical Function on Urinary Alphaketolic Steroid Metabolites 1

The Effect of Potassium Deficiency Upon Adrenocortical Secretion in the Rat 1

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