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First published online May 5, 2005
Journal of Experimental Biology 208, 1927-1935 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01606
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Cardiac preload and venous return in swimming sea bass (Dicentrarchus labrax L.)

Erik Sandblom1,*, Anthony P. Farrell2, Jordi Altimiras3, Michael Axelsson1 and Guy Claireaux4

1 Department of Zoology, Göteborg University, Box 463, S-405 30 Göteborg, Sweden
2 Faculty of Agricultural Sciences and Department of Zoology, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada
3 Department of Biology, Institute of Physics and Measurement Technology, Linköpings Universitet, S-58183 Linköping, Sweden
4 Centre de Recherche sur les Ecosystèmes Marins et Aquacoles (CNRS-IFREMER), Place du Séminaire, F-17137, L'Houmeau, France

* Author for correspondence (e-mail: erik.sandblom{at}zool.gu.se)

Accepted 15 March 2005

Cardiac preload (central venous pressure, PCV), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (PDA) and relative cardiac output () were measured in sea bass (Dicentrarchus labrax) at rest and while swimming at 1 and 2 BL s-1. MCFP, an index of venous capacitance and the upstream venous pressure driving the return of venous blood to the heart, was measured as the plateau in PCV during ventral aortic occlusion. Compared with resting values, swimming at 1 and 2 BL s-1 increased (by 15±1.5 and 38±6.5%, respectively), PCV (from 0.11±0.01 kPa to 0.12±0.01 and 0.16±0.02 kPa, respectively), MCFP (from 0.27±0.02 kPa to 0.31±0.02 and 0.40±0.04 kPa, respectively) and the calculated pressure gradient for venous return ({Delta}PV, from 0.16±0.01 kPa to 0.18±0.02 and 0.24±0.02 kPa, respectively), but not PDA. In spite of an increased preload, the increase in was exclusively mediated by an increased heart rate (fH, from 80±4 beats min-1 to 88±4 and 103±3 beats min-1, respectively), and stroke volume (Vs) remained unchanged. Prazosin treatment (1 mg kg-1 Mb) abolished pressure and flow changes during swimming at 1 BL s-1, but not 2 BL s-1, indicating that other control systems besides an {alpha}-adrenoceptor control are involved. This study is the first to address the control of venous capacitance in swimming fish. It questions the generality that increased during swimming is regulated primarily through Vs and shows that an increased cardiac filling pressure does not necessarily lead to an increased Vs in fish, but may instead compensate for a reduced cardiac filling time.

Key words: cardiac preload, cardiac output, exercise, heart rate, mean circulatory filling pressure, prazosin, sea bass, stroke volume, teleost, venous capacitance, venous return




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