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 Google Scholar
Google Scholar
Right arrow Articles by Nye, C. E.
Right arrow Articles by Roberts, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nye, C. E.
Right arrow Articles by Roberts, J.
Journal of Pharmacology And Experimental Therapeutics, Vol. 152, Issue 1, 67-74, 1966
Copyright © 1966 by American Society for Pharmacology and Experimental Therapeutics


THE REACTIVITY OF ATRIAL AND VENTRICULAR PACEMAKERS TO QUINIDINE

Charles Erik Nye 1 and Jay Roberts 1

1 Department of Pharmacology, Cornell University Medical College, New York, New York

The sensitivity of atrial and ventricular pacemakers to the depressant actions of quinidine was determined in isolated cat hearts with surgically induced heart block. Quinidine administered by single injection or by perfusion caused a greater slowing of the atrial rate than of the ventricular rate. The greater sensitivity of the atrial pacemaker to quinidine was also indicated by the finding that the ventricular pacemaker completely recovered from quinidine depression while the atrial pacemaker failed to recover fully. There was also a greater incidence of rhythm disturbances in the atrium than in the ventricle. It may be possible to explain the greater sensitivity of the atrial pacemaker to quinidine depression by the fact that its rate of firing is greater than that of the ventricle. A faster rate of firing of an abnormal focus may also explain, at least in part, the observation that ventricular tachycardia can be successfully converted to normal sinus rhythm by quinidine. Regardless of the method of administration or the concentration used, quinidine did not accelerate the atrial or ventricular rate. This suggested that the accleration of the heart rate by quinidine in vivo depends on an intact sympathetic nervous system.

Accepted on October 19, 1965







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

Copyright © 1966 by the American Society for Pharmacology and Experimental Therapeutics.