The Effect of the Subcutaneous Injection of Adrenalin on the Leukocyte Count of Splenectomized Patients and of Patients With Certain Diseases of the Hematopoietic and Lymphatic Systems

Lucia, S. P.; Leonard, Maurice; Falconer, Ernest H.

doi:10.1097/00000441-193707000-00004

Cited by 20 publications

(2 citation statements)

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“…This appears unrelated to the initial eosinophilia, which accompanies a rise in all white cell elements, one half to one hour after the injection (30). In man, the administration of more than 0.3 mg. of epinephrine produces a fall in eosinophils of 50 to 70 per cent.…”

Section: Discussionmentioning

confidence: 93%

Studies on the Effect of Epinephrine on the Pituitary-Adrenocortical System*

Recant

Hume

Forsham

et al. 1950

The Journal of Clinical Endocrinology & Metabolism

159

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T N 1908, Babes and Jonescu observed that conditions of stress in man X and laboratory animals were associated with the depletion of suprarenal lipid. Multiple intravenous injections of epinephrine produced a similar depletion, accompanied by adrenal hypertrophy in rabbits (1). Vogt later demonstrated that following the administration of epinephrine, cortical hormones could be detected in the adrenal venous blood of cats and dogs (2). Long and Fry (3) studied this response of the adrenal cortex to epinephrine, using the assay of Sayers (4) for adrenal corticotropic hormone (ACTH). They described a significant ACTH release in response to injected epinephrine in normal rats; on the other hand, hypophysectomized rats failed to show this response, in spite of the fact that their adrenal cortices were maintained with exogenous pituitary hormone injections. From these data Long postulated that the effect of epinephrine on the adrenal cortex was mediated by the pituitary. Vogt subsequently reported similar differences between hypophysectomized and normal rats in response to epinephrine (5). This work provided additional support to the postulation of the mediatory role of the pituitary in the adrenal cortical changes induced by epinephrine.Selye pointed out the physiologic integration of neuro-endocrine responses to stress in his description of the general adaptation syndrome (6). He showed that adaptation is largely dependent upon the initial sympathetic reaction of the body to nonspecific stimuli. This reaction is then succeeded by the mobilization of the pituitary and adrenal cortical hormones. Epinephrine release affords the immediate protection, while the adrenal cortical hormones provide more sustained effects. The sequence of these reactions suggests a coordinating mechanism. Although epinephrine appears to be an important link in this integrated system, it has not been demonstrated conclusively to act upon the anterior pituitary, nor has it

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Section: Discussionmentioning

confidence: 93%

Studies on the Effect of Epinephrine on the Pituitary-Adrenocortical System*

Recant

Hume

Forsham

et al. 1950

The Journal of Clinical Endocrinology & Metabolism

159

View full text Add to dashboard Cite

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“…Based on these investigations, Frey concluded that epinephrine caused a "contraction" of the spleen, resulting in a mechanical efflux of lymphoid cells. This finding was questioned by others who observed epinephrine-induced lymphocytosis in splenectomized animals (Edmunds and Stone, 1924) and humans (Patek and Daland, 1935;Lucia et al, 1937). The observations made by Frey in freshly splenectomized subjects were also challenged by others who observed positive responses in asplenic subjects (Grimm, 1919;Hess, 1922, as cited in Benschop et al, 1996.…”

Section: Plasma Catecholamines and Immune Functionmentioning

confidence: 96%

Splenic Contraction, Catecholamine Release, and Blood Volume Redistribution During Exercise in Man

Stewart

Hodges

McKenzie

2002

Medicine & Science in Sports & Exercise

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Ill response to an intensity dependent signal and that sympathetic stimulation, as reflected in changes in plasma catecholamine concentrations, is involved in this effect. In a simultaneous study, the effect of splenic contraction during exercise on the circulating red cell volume and indirect calculations of plasma volume change (Hb/Hct) was determined. Radio nuclide measurements of red cell and plasma volume were performed, and a blood count taken, prior to and immediately following exercise. The release of 50 mis of red cells from the spleen during exercise accounted for a 2.2% increase in the total circulating red cell volume. The indirect calculations of plasma volume were unaffected by the minor increase in peripheral hematocrit and were equivalent to radio labelled measurements. In conjunction the results of this dissertation imply that the release of red cells during exercise is not a primary function of the human spleen.

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