JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
 QUICK SEARCH:   [advanced]


     


Anesth Analg 1977; 56:46-54
© 1977 International Anesthesia Research Society
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by ANTON, A. H.
Right arrow Articles by REDDERSON, C. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by ANTON, A. H.
Right arrow Articles by REDDERSON, C. L.

Autonomic Blockade and the Cardiovascular and Catecholamine Response to Electroshock

A. H. ANTON, PhD*, D. S. UY, MD{dagger}, and C. L. REDDERSON, MD{ddagger}

* Professor of Anesthesiology and Pharmacology., Department of Anesthesiology, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, Ohio 44106. {dagger} Resident in Anesthesiology., Department of Anesthesiology, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, Ohio 44106. {ddagger}Assistant Professor of Anesthesiology., Department of Anesthesiology, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, Ohio 44106.

Abstract

From a study on the interrelationship between electroshock-induced convulsions, autonomie function, catecholamines, and cardiovascular homeostasis in dogs, the authors found that: (1) the asystole of electroshock (ES) was significantly prolonged by high spinal anesthesia but not by relative alpha- or beta-adrenergic blockade; (2) increased levels of circulating catecholamines were solely responsible for the marked hypertensive response to ES, since the pressor effect could be blocked by preventing the release of catecholamines with high spinal anesthesia or by inhibiting alpha-adrenergic receptors with phenoxybenzamine; (3) the adrenal medulla appeared to be the source of most of the ES-induced increase in circulating catecholamines; (4) the asystole and arrhythmias of ES were a cholinergic effect, since they were blocked by atropine; (5) there was a dose-response relationship between the coulombs of electricity administered and the catecholamine and cardiovascular responses; and (6) that the adverse cardiovascular effects of ES therapy could be ameliorated pharmacologically.




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
D. H. van Zijl, P. C. Gordon, and M. F. James
The Comparative Effects of Remifentanil or Magnesium Sulfate Versus Placebo on Attenuating the Hemodynamic Responses After Electroconvulsive Therapy
Anesth. Analg., December 1, 2005; 101(6): 1651 - 1655.
[Abstract] [Full Text] [PDF]


Home page
Anesth. Analg.Home page
L. D. Wright, D. E. Martin, and T. L. Tan
Response to Electroconvulsive Therapy in a Quadriplegic Patient
Anesth. Analg., December 1, 1999; 89(6): 1409 - 1409.
[Full Text] [PDF]




Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 1977 by the International Anesthesia Research Society.