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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HYMAN, A. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HYMAN, A. L.
Journal of Pharmacology And Experimental Therapeutics, Vol. 165, Issue 2, 267-273, 1969
Copyright © 1969 by American Society for Pharmacology and Experimental Therapeutics


THE ACTIVE RESPONSES OF PULMONARY VEINS IN INTACT DOGS TO PROSTAGLANDINS F2 ALPHA AND E1

ALBERT L. HYMAN 1

1 Cardiopulmonary Laboratory, Department of Surgery, Tulane University School of Medicine, New Orleans, Louisiana

The direct response of the pulmonary veins to prostaglandins (PGF2agr) and E1 (PGE1) in intact dogs was studied by a technique of pump perfusion of a hemodynamically separated lobar artery at a constant rate of flow. During administration of these agents, their direct effects were studied in the vessels of the pump-perfused lobe, while the modulated effects were studied in the vessels of the normally perfused lobes. In the pump-perfused lobe, PGF2agr abruptly increased lobar arterial pressure and more slowly increased lobar venous pressure. These data indicate that PGF2agr actively constricts the lobar vein and vessels upstream to the venous segment, presumably the lobar arteries. The data additionally suggest that the progressively increasing venous constriction may modify the direct constrictor effect on the upstream vessels. Since flow through the normally perfused vessels was not significantly (P > .5) altered, the increase in pressure in the main pulmonary artery indicates that vessels in these lobes also constricted. PGE1 caused active dilation of the lobar veins and upstream vessels. The response was slower than the response to PGF2agr but was progressive during a 10-min infusion. Since both flow and pressure in the normally perfused lobes simultaneously decreased during PGE1 infusion, the direct effect of this agent on normally perfused lobes was obscured.

Submitted on July 3, 1968
Accepted on October 17, 1968




This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
T. Suzuki, Y. Fujii, M. Miyano, L.-Y. Chen, T. Takahashi, and K. Watanabe
cDNA Cloning, Expression, and Mutagenesis Study of Liver-type Prostaglandin F Synthase
J. Biol. Chem., January 1, 1999; 274(1): 241 - 248.
[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 © 1969 by the American Society for Pharmacology and Experimental Therapeutics.