AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 246: H351-H359, 1984;
0363-6135/84 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Gustafsson, D.
Right arrow Articles by Lundvall, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gustafsson, D.
Right arrow Articles by Lundvall, J.

AJP - Heart and Circulatory Physiology, Vol 246, Issue 3 351-H359, Copyright © 1984 by American Physiological Society


ARTICLES

Beta 2-adrenergic vascular control in hemorrhage and its influence on cardiac performance

D. Gustafsson and J. Lundvall

Cardiac output (CO), heart rate, stroke volume (SV), and total peripheral resistance (TPR) were followed in anesthetized cats with intact and selectively blocked beta 2-adrenoceptors. SV and CO decreased and TPR increased initially after bleeding in both groups. After this, animals with intact beta 2-adrenoceptors showed gradual recovery of SV and CO and gradual restoration to control of the initially raised TPR. In beta 2-blocked animals SV and CO instead remained low and TPR high. These patterns of response occurred after mild, moderate, and severe bleeding. Separate experiments indicated that the restoration of TPR with intact beta 2-adrenoceptors mainly can be attributed to beta 2-adrenergic dilator interaction with the vasoconstrictor influences. The previously described beta 2-adrenergic control of plasma volume in hemorrhage (Acta Physiol. Scand. 116: 175-180, 1982) suggests that the increases in SV and CO with intact beta 2-adrenoceptors, in turn, probably are indirect effects on cardiac performance due to improved cardiac filling. A synthesis of present and previous findings thus suggests the existence of a beta 2-adrenergic vascular control in hemorrhage favoring tissue perfusion via decreased resistance and via increased plasma volume and hence SV and CO.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online