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First published online March 17, 2006
Journal of Experimental Biology 209, 1310-1325 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02105
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Cardiorespiratory modifications, and limitations, in post-smolt growth hormone transgenic Atlantic salmon Salmo salar

E. J. Deitch, G. L. Fletcher, L. H. Petersen, I. A. S. F. Costa, M. A. Shears, W. R. Driedzic and A. K. Gamperl*

Ocean Sciences Centre, Memorial University of Newfoundland, St John's, Newfoundland A1C 5S7, Canada


Figure 1
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  		Fig. 1. Identification of GH transgenic and control Atlantic salmon using polymerase chain reaction (PCR). All samples were analyzed by electrophoresis using a 2% agarose gel and visualized with ethidium bromide. A water control was run to ensure that no exogenous genetic material was present in the samples and a positive control indicated the position of the transgene. *Band of 207 bp indicates presence of the transgene; {dagger}banding representative of the endogenous Atlantic salmon GH genes, GH1 (1150 bp) and GH2 (798 bp).

 

Figure 2
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  		Fig. 2. Experimental protocol for measuring Qmax and power output of the in situ Atlantic salmon heart. The broken line represents the end-diastolic pressure developed by the ventricle, determined by adjusting the height of the output pressure head. Pout was normally set to a physiologically realistic value of 5 kPa; however a subphysiological level of Pout (2–3 kPa) was used at the start of the protocol to let the heart recover from surgery. The first set of steps indicate the maximum cardiac output test (Qmax), where Pin was raised sequentially from 0.15 kPa to 0.6 kPa, whereas the second set of steps indicate the myocardial power test where output pressure was raised from 3 kPa to 10 kPa, while Pin remained at 0.60 kPa.

 

Figure 3
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  		Fig. 3. Oxygen consumption of transgenic (open circles, y=–9.88+174.92x+9.17x2) and control (closed circles, y=–18.27+147.49x+21.95x2) Atlantic salmon at various swimming speeds. Values are means ± 1 standard error (N=8).

 

Figure 4
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  		Fig. 4. Relationships between routine oxygen consumption and total gill surface area for transgenic (open circles, y=–0.02+0.98x, R2=0.63, P=0.02) and control (closed circles, y=1.26+0.25x, R2=0.10, P=0.50) Atlantic salmon (N=8).

 

Figure 5
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  		Fig. 5. The effect of increased input pressure (kPa) on maximum in situ stroke volume (A, ml kg–1) (B, ml g ventricle–1) of transgenic and control Atlantic salmon hearts. (A) Transgenic salmon (N=7) are represented by open circles (y=0.36+0.14x–0.002x2, R2=0.98) and controls (N=8) are represented by closed circles (y=0.43+0.11x–0.002x2, R2=0.99). (B) Transgenic salmon are represented by open circles (y=0.45+0.18x–0.003x2, R2=0.99) and controls are represented by closed circles (y=0.64+0.17x–0.003x2, R2=0.99). Curves were fitted using second order regressions. Values are means ± 1 standard error.

 

Figure 6
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  		Fig. 6. The effect of increased output pressure (kPa) on myocardial power output (mW g–1 ventricle) of in situ transgenic (open circles, y=–13.2+0.71x–6.91x2+1.83x3, R2=0.95) and control (closed circles y=–14.2+0.75x–7.2x2+1.83x3, R2=0.98) Atlantic salmon hearts. Hearts were left at the Pin at which Qmax was obtained while Pout was being manipulated. Curves were fitted using a second order regression. Values are means ± 1 standard error (N=7 for transgenic salmon; N=8 for controls).

 

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© The Company of Biologists Ltd 2006