You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 28 No. 1, January 1973 TABLE OF CONTENTS
  Archives
  •  Online Features
  ORIGINAL CONTRIBUTIONS
 This Article
 •References
 •Full text PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Protective Adaptation of Brain to Water Intoxication

Marilyn M. Rymer, MD; Robert A. Fishman, MD

Arch Neurol. 1973;28(1):49-54.


Abstract

An animal model of inappropriate antidiuretic hormone secretion was used to study changes in water and electrolytes in water intoxication. As the serum became hypotonic, brain and muscle initially reacted by swelling and decreasing sodium content. Subsequently, muscle continued to swell and maintained normal potassium levels. Brain decreased its dry weight potassium content by 20% and swelled half as much as muscle. The critical factor in determination of consciousness was the level of brain water, not the level of sodium or potassium. Grey and white matter were affected equally. Permeability to mannitol was normal in the experimental model. Corticosteroids were found to have no effect on the syndrome. The drop in brain potassium level is interpreted as a protective adaptation to prevent massive swelling as occurred in muscle.



Author Affiliations

San Francisco

From the Department of Neurology, University of California, San Francisco. Dr. Rymer is now with the University of Wisconsin Hospitals, Madison.


Footnotes

Accepted for publication July 31, 1972.

Read in part before the 1972 meeting of the American Academy of Neurology, St. Louis, April 26, 1972.

Reprint requests to Department of Neurology, University of California San Francisco, Third Ave and Parnassus, San Francisco, Calif 94122 (Dr. Fishman).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Sodium potassium adenosine triphosphatase activity in preterm and term infants and its possible role in sodium homeostasis during maturation
Bistritzer et al.
Arch. Dis. Child. Fetal Neonatal Ed. 1999;81:184F-187.
ABSTRACT | FULL TEXT  

Hypoxia Is the Cause of Brain Damage in Hyponatremia
Knochel
JAMA 1999;281:2342-2343.
FULL TEXT  

Compulsive Water Drinking in Infants and Young Children
Horev and Cohen
CLIN PEDIATR 1994;33:209-213.
ABSTRACT  

Fatal Central Diabetes Mellitus and Insipidus Resulting from Untreated Hyponatremia: A New Syndrome
Fraser and Arieff
ANN INTERN MED 1990;112:113-119.
ABSTRACT  

Severe Diuretic-Induced Hyponatremia in the Elderly: A Series of Eight Patients
Ashouri
Arch Intern Med 1986;146:1355-1357.
ABSTRACT  

Transient Hyperthyroxinemia in Symptomatic Hyponatremic Patients
Cogan and Abramow
Arch Intern Med 1986;146:545-547.
ABSTRACT  

The Sink Action of Cerebrospinal Fluid Volume Flow: Effect on Brain Water Content
Hochwald et al.
Arch Neurol 1976;33:339-344.
ABSTRACT  

Pathogenesis of Lead Encephalopathy: Uptake of Lead and Reaction of Brain Capillaries
Goldstein et al.
Arch Neurol 1974;31:382-389.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1973 American Medical Association. All Rights Reserved.