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      Activation of the Adrenocortical Axis by Surgical Stress: Involvement of Central Norepinephrine and Interleukin-1

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          Abstract

          In the present study, we examined the mechanisms involved in the activation of the adrenocortical axis following surgical stress. Adult male rats underwent surgical laparotomy or craniotomy under ether anesthesia while control rats were only ether-anesthetized. Four hours following laparotomy or craniotomy, serum adrenocorticotropin (ACTH) and corticosterone (CS) were significantly increased and returned to almost basal levels after 24 h. Laparotomy also caused a significant depletion of corticotropin-releasing hormone (CRH-41) in the median eminence (ME). Pretreatment with dexamethasone 50 μg/kg completely abolished the pituitary-adrenal response while pretreatment with type II corticosteroid receptor antagonist caused a significant hypersecretion of both ACTH and CS and inhibited the effect of dexamethasone. The response to laparotomy was markedly attenuated in rats injected with 6-hydroxydopamine into the paraventricular nucleus (PVN) which significantly depletes norepinephrine (NE) PVN content. Intracerebroventricular injection of interleukin-1 receptor antagonist (IL-1ra) also inhibited the pituitary-adrenal response to laparotomy. The results suggest that (1) surgical stress activates the hypothalamo-pituitary-adrenal (HPA) axis via a mechanism which involves the release of CRH from the ME and NE input to the PVN; (2) the adrenocortical response is sensitive to the negative feedback of glucocorticoids via the mediation of type II glucocorticoid receptors, and (3) central IL-1 may be a mediator in the HPA axis response to surgical stress.

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          Most cited references 4

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          Immobilization stress induces interleukin-1β mRNA in the rat hypothalamus

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            Abnormal cytokine serum levels correlate with impaired cellular immune responses after surgery.

            Serum levels of the interleukins (IL)-2, -1 beta, and -6, tumor-necrosis factor alpha (TNF-alpha), and prostaglandin E2 (PGE2) were measured serially before and after operation in patients undergoing various surgical procedures. Peripheral blood mononuclear cells (PBMC) from the same patients were analyzed before and after surgery for proliferative responses in the autologous mixed lymphocyte reaction (AMLR) and for cytolytic activity against the natural killer (NK)-sensitive K562 cell line. In patients who had major surgery, a decrease in IL-2 levels and increases in IL-1 beta, TNF-alpha, IL-6, and PGE2 levels were observed up to 9 days after the operation compared to those of the preoperative values. Decreased AMLR responses and NK activity were also observed in PBMC collected 5 days after surgery. All these changes were more intense in patients who had undergone major surgical procedures of increasing severity (i.e., cancer patients). Similar, although weaker, changes in cytokine serum levels, AMLR responses, and NK activity were also observed in patients undergoing minor surgery. Our data suggest that changes in cytokine serum levels may cause cellular immune dysfunctions, particularly in patients undergoing major surgery, and provide the basis for immune intervention in order to avoid infections occurring after major surgery.
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              Evidence for the involvement of the central adrenergic system in interleukin 1-induced adrenocortical response.

              The role of central catecholamines in the mediation of adrenocortical activation, induced by interleukin 1 (IL-1), was investigated by measuring ACTH and corticosterone in serum. Adult male rats were injected with either vehicle or the neurotoxin 6-hydroxydopamine (6-OHDA) into the lateral ventricle or the ventral noradrenergic ascending bundle. In vehicle-injected rats, 2 U of IL-1, injected intraventricularly, produced a 5- and 15-fold increase in ACTH and CS, respectively, in serum, 120 min after the injection of IL-1. In contrast, 6-OHDA, injected either intraventricularly or into the ventral noradrenergic ascending bundle, abolished the response to an intracerebral injection of IL-1. In addition, in rats pretreated with the alpha 1-adrenergic antagonist, prazosin, IL-1 failed to activate the adrenocortical axis. In other rats pretreated with the beta-adrenergic antagonist, propranolol, the adrenocortical response did not significantly differ from that of vehicle-pretreated rats. These results suggest that central adrenergic transmission, originating at the ventral noradrenergic ascending bundle and acting through alpha 1-adrenergic receptors, is involved in the adrenocortical response to IL-1.
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2000
                May 2000
                04 May 2000
                : 7
                : 4
                : 182-188
                Affiliations
                aSchool of Nursing and bDepartment of Neurology, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel
                Article
                26437 Neuroimmunomodulation 2000;7:182–188
                10.1159/000026437
                10810250
                © 2000 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 5, References: 33, Pages: 7
                Categories
                Original Paper

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