JPET Celsis microsomes equal better data

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 Nakano, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakano, J.
Journal of Pharmacology And Experimental Therapeutics, Vol. 157, Issue 1, 19-31, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics


STUDIES ON THE CARDIOVASCULAR EFFECTS OF SYNTHETIC VASOPRESSIN

Jiro Nakano 1

1 Department of Pharmacology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma

The effects of lysine-8-vasopressin (LVP) on the cardiovascular dynamics and myocardial oxygen metabolism were studied in anesthetized, open-chest dogs. It was found that the i.v. administration of 1 to 125 mU/kg of LVP decreased heart rate, pulmonary arterial pressure, cardiac output, systemic venous return and coronary blood flow. In addition, LVP increased mean systemic arterial pressure, left atrial pressure, left ventricular systolic and diastolic pressures, and total, pulmonary and coronary peripheral resistances essentially in proportion to the dose given. Furthermore, LVP decreased myocardial oxygen uptake, myocardial contractility and left ventricular performance. It is concluded that the reduction in cardiac output and left ventricular performance is most likely due to the decreased myocardial contractile force induced by the direct coronary constriction, to the marked increase in total peripheral resistance, and also to the decrease in the systemic venous return caused by the increased total peripheral capacitance. LVP decreased pulmonary arterial pressure owing to the marked decrease in right ventricular output which was induced by the decrease in systemic venous return and right ventricular contractile force in spite of the increase in left atrial pressure and pulmonary peripheral resistance. LVP tachyphylaxis and catecholamine hypersensitivity after LVP can be explained partially by the prolonged hemodynamic effects of LVP, especially in regard to its effect on the total peripheral capacitance.

Submitted on October 27, 1966
Accepted on January 16, 1967







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.