Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Anderson, D. K.
Right arrow Articles by Green, E. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Anderson, D. K.
Right arrow Articles by Green, E. S.
NEUROLOGY 1983;33:722
© 1983 American Academy of Neurology

Susceptibility of feline spinal cord energy metabolism to severe incomplete ischemia

Douglas K. Anderson, PhD, Michael M. Behbehani, PhD, Eugene D. Means, MD, Thomas R. Waters, MS and Evangelyn S. Green, BA

Veterans Administration Medical Center and Departments of Neurology and Physiology, University of Cincinnati College of Medicine, Cincinnati, OH.

Feline spinal cords were subjected to 10 to 30 minutes of severe incomplete ischemia (average reduction in blood flow of 92%) with and without 90 minutes of recirculation, and the L-2 segment was analyzed for high-energy phosphates and certain glycolytic metabolites. Spinal cord tissue lactic acid levels were stepwise elevated, and adenosine triphosphate (ATP), phosphocreatine (P-creatine), and glucose were progressively consumed by increasing durations of ischemia. However, upon restoration of blood flow, there was extensive recovery of energy metabolites and normalized lactic acid, demonstrating resumption of mitochondrial oxidative metabolism. These data indicate that the spinal cord can tolerate at least 30 minutes of severely reduced blood flow before recovery of energy metabolism is significantly impaired upon restitution of blood flow.

Address correspondence and reprint requests to Dr. Anderson, Veterans Administration Medical Center, Neurology Service (127),3200 Vine Street, Cincinnati, OH 45220.

This work was supported by the Veterans Administration.

A preliminary report of this work was presented at the thirty-third annual meeting of the American Academy of Neurology, Toronto, Canada, 1981.

Accepted for publication September 28, 1982.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1983 by AAN Enterprises, Inc.