|Author(s)||Sandblom Erik1, Farrell Anthony2, Altimiras Jordi3, Axelsson Michael1, Claireaux Guy4, 5|
|Affiliation(s)||1 : Univ Gothenburg, Dept Zool, S-40530 Gothenburg, Sweden.
2 : Univ British Columbia, Fac Agr Sci, Vancouver, BC V6T 1Z4, Canada.
3 : Linkoping Univ, Inst Phys & Measurement Technol, Dept Biol, S-58183 Linkoping, Sweden.
4 : IFREMER, CNRS, Ctr Rech Ecosyst Marins & Aquacoles, F-17137 Lhoumeau, France.
|Source||The Journal of Experimental Biology (0022-0949) (The Company of Biologists), 2005-05 , Vol. 208 , N. 10 , P. 1927-1935|
|WOS© Times Cited||36|
|Keyword(s)||Blood pressure, Cardiac rythm, Swimming aquaculture, Sea bass|
|Abstract||Cardiac preload (central venous; pressure, Pcv), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (P-DA) and relative cardiac output (Q) 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 2BL s(-1) increased Q (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 0 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 (V-s) remained unchanged. Prazosin treatment (1 mg kg(-1) M-b) 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 Q during swimming is regulated primarily through V-s and shows that an increased cardiac filling pressure does not necessarily lead to an increased V-s in fish, but may instead compensate for a reduced cardiac filling time.|
Sandblom Erik, Farrell Anthony, Altimiras Jordi, Axelsson Michael, Claireaux Guy (2005). Cardiac preload and venous return in swimming sea bass (Dicentrarchus labrax L.). The Journal of Experimental Biology, 208(10), 1927-1935. Publisher's official version : https://doi.org/10.1242/jeb.01606 , Open Access version : https://archimer.ifremer.fr/doc/00000/421/