JPET Introducing ALZET?ew Model 2006 Pump

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 Google Scholar
Google Scholar
Right arrow Articles by YU, D. H.
Right arrow Articles by GLUCKMAN, M. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by YU, D. H.
Right arrow Articles by GLUCKMAN, M. I.
Journal of Pharmacology And Experimental Therapeutics, Vol. 170, Issue 1, 37-43, 1969
Copyright © 1969 by American Society for Pharmacology and Experimental Therapeutics


THE EFFECT OF DIPYRIDAMOLE ON THE METABOLISM OF CARDIAC MUSCLE

DAI HYON YU 1 and M. I. GLUCKMAN 1

1 Department of Pharmacology, Wyeth Laboratories Inc., Radnor, Pennsylvania

The relationship between the metabolic and inotropic effect of dipyridamole on in vitro preparations of cat papillary and left atrial muscles was investigated. The oxygen consumption, contractility, glycogen content and energy-rich phosphate levels were used as parameters. They were measured by techniques previously described by Lee et at. (1960). Dipyridamole had no effect on the oxygen consumption of resting muscle. However, it increased both the contractility and oxygen consumption of electrically stimulated muscle, an increase in contractility occurring before oxygen consumption changed. Dipyridamole did not increase the mechanical efficiency of fresh, contracting papillary muscle; however, it did cause an apparent increase with atrial muscle. Dipyridamole did not significantly change the tissue content of either glycogen or energy-rich phosphate compounds. Both pronethalol and reserpine pretreatment were found to block dipyridamole's inotropic effect. From the above data, it is concluded that the increase in oxygen consumption after dipyridamole is a consequence of the increased contractility and furthermore, based on the interaction with reserpine and pronethalol, that dipyridamole increases contractility through an adrenergic mechanism.

Submitted on April 23, 1969
Accepted on August 3, 1969







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

Copyright © 1969 by the American Society for Pharmacology and Experimental Therapeutics.