JPET

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Hinshaw, L. B.
Right arrow Articles by Gunter, B. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hinshaw, L. B.
Right arrow Articles by Gunter, B. J.
Journal of Pharmacology And Experimental Therapeutics, Vol. 157, Issue 3, 665-671, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics

EFFECTS OF ACETYLSALICYLIC ACID ON THE CANINE RESPONSE TO ENDOTOXIN

L. B. Hinshaw 1, L. A. Solomon 1, E. G. Erdös 1, D. A. Reins 1, and B. J. Gunter 1

1 Veterans Administration Hospital, and Departments of Physiology, Pharmacology and Surgery, University of Oklahoma Medical Center, Oklahoma City, Oklahoma

The acute response of the dog to a lethal injection of endotoxin is characterized by portal pooling, decreased venous return and systemic arterial hypotension aecompanied by acidosis and hemoconcentration. This paper describes effects of acetylsalicylic acid (ASA) on the hemodynamic and survival responses to endotoxin. Adult mongrel dogs of either sex were anesthetized with i.v. sodium pentobarbital and infused with buffered or unbuffered ASA (100 mg/kg and 40-50 mg/kg, respectively) before or after the injection of an LD80 dose of Escherichia coli endotoxin. The action of ASA alone resulted in increased cardiac output and decreased total peripheral resistance. Pretreatment with ASA blocked acute responses to endotoxin: portal hypertension did not occur, venous return and systemic arterial pressure remained significantly elevated and acidosis was prevented. The prevention of the decreases in cardiac output and systemic arterial pressure by ASA is primarily attributed to obliteration of hepatic pooling. Posttreatment restored systemic arterial pressure and pH to control values. Pretreatment with buffered and unbuffered ASA prior to endotoxin injection significantly increased survival rate over the untreated controls given endotoxin alone. These data suggest that the lethal effects of endotoxin are related to its hemodynamic alterations.

Submitted on January 12, 1967
Accepted on April 27, 1967




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
G. Y. Park and J. W. Christman
Involvement of cyclooxygenase-2 and prostaglandins in the molecular pathogenesis of inflammatory lung diseases
Am J Physiol Lung Cell Mol Physiol, May 1, 2006; 290(5): L797 - L805.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
G. R. Bernard, A. P. Wheeler, J. A. Russell, R. Schein, W. R. Summer, K. P. Steinberg, W. J. Fulkerson, P. E. Wright, B. W. Christman, W. D. Dupont, et al.
The Effects of Ibuprofen on the Physiology and Survival of Patients with Sepsis
N. Engl. J. Med., March 27, 1997; 336(13): 912 - 918.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics.