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. 26 No. 1, January 1972 TABLE OF CONTENTS
  Archives
  •  Online Features
  ORIGINAL ARTICLES
 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
 •Citing articles on Web of Science (58)
 •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?

Cerebral Water and Electrolytes

An Experimental Model of Inappropriate Secretion of Antidiuretic Hormone

Carl J. Dila, MD; Hanna M. Pappius, PhD

Arch Neurol. 1972;26(1):85-90.


Abstract

Administration of fluid and vasopressin injection to rats induced within 24 to 48 hours a condition which can be considered as an experimental model of the syndrome of inappropriate secretion of antidiuretic hormone (ADH). Concurrently with hyponatremia and hypoosmolarity in serum, the changes in muscle consisted of a fall in sodium content and a decrease in percentage dry weight equivalent to 12% swelling. There was no loss of potassium from muscle. In contrast, in brain the decrease in sodium content was smaller, the tissue percentage dry weight decreased only slightly, indicating minimal swelling, and there was a significant net loss of potassium. It is suggested that neurological dysfunction associated with the syndrome of inappropriate secretion of ADH is unlikely to be due to cerebral edema but may be related to the decreased potassium content of brain tissue.



Author Affiliations

Montreal

From the Donner Laboratory of Experimental Neurochemistry, Montreal Neurological Institute, and the Department of Neurology and Neurosurgery, McGill University, Montreal.


Footnotes

Accepted for publication June 9, 1971.

Reprint requests to Donner Laboratory of Experimental Neurochemistry, Montreal Neurological Institute, 3801 University St, Montreal 112 (Dr. Pappius).



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  

Severe Symptomatic Hyponatremia: Treatment and Outcome: A Study of 64 Cases
STERNS
ANN INTERN MED 1987;107:656-664.
ABSTRACT  

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

Rapid correction of hyponatremia causes demyelination: relation to central pontine myelinolysis
Kleinschmidt-DeMasters and Norenberg
Science 1981;211:1068-1070.
ABSTRACT  

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

Protective Adaptation of Brain to Water Intoxication
Rymer and Fishman
Arch Neurol 1973;28:49-54.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1972 American Medical Association. All Rights Reserved.