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First published online June 16, 2004
Journal of Experimental Biology 207, 2539-2550 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01057

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Cardiac plasticity in fishes: environmental influences and intraspecific differences

A. Kurt Gamperl^1,* and A. P. Farrell²

¹ Ocean Sciences Center, Memorial University of Newfoundland, St John's, Newfoundland, Canada A1C 5S7
² Department of Biological Sciences, 8888 University Drive, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6

View larger version (16K): [in a new window]   Fig. 1. For swimming studies, a tight relationship exists between maximum oxygen uptake (O2max) and maximum arterial oxygen transport (O2max; the product of maximum cardiac output and arterial oxygen carrying capacity) among a variety of fish species (O2max=0.84 O2max–4.03; r2=0.99). These data also illustrate the modest increase in both O2max and O2max produced with intense exercise training in chinook salmon. C, control; Tr, exercise-trained; Co, Atlantic cod, Gadus morhua; L, leopard shark; D, dogfish; R1+R2, rainbow trout). Graph taken with permission from Gallaugher et al. (2001).

View larger version (99K): [in a new window]   Fig. 2. Photographs of teleost hearts to illustrate normal and abnormal morphology. (A) Normal heart from a wild steelhead trout Oncorhynchus mykiss (5 kg) from Idaho. Note the typical sharp edges to the pyramidal ventricle, and that the coronary arteries are not obvious. (B) An abnormal heart from a farmed rainbow trout Oncorhynchus mykiss (3 kg), which died suddenly in an aquaculture pen in Norway. Note the more rounded shape to the ventricle, and the more superficial (prominant) coronary arteries. (C) An abnormal heart from a farmed Atlantic salmon Salmo salar (4 kg), which died suddenly in an aquaculture pen in Norway. Note the excess fat deposits on the surface of the bulbus arteriosus and ventricle. Photographs A–C were provided courtesy of Dr Trygve Poppe. (D) An abnormal heart from a farmed sea bass Dicentrachus labrax (1.4 kg), which died suddenly in an aquaculture pen in France. Note the deformed shapes of the bulbus arteriosus and ventricle. (E) A normal heart from a farmed triploid brown trout Salmo trutta (400 g) taken from an aquaculture pen in France. Note the acute angle subtended by the bulbus arteriosus to the ventricle. (F) An abnormal heart from a farmed triploid brown trout Salmo trutta (500 g). Note the extreme angle subtended by the bulbus arteriosus to the ventricle. Photographs D–F were provided courtesy of Dr Guy Claireaux.

View larger version (17K): [in a new window]   Fig. 3. Recovery of cardiac function following 30 min of severe hypoxia, measured as the percentage recovery of maximum force by ventricular strips [Gesser, 1977; open circles, rainbow trout (N=5) and closed circles, carp (N=5)], or as the % recovery of MAX in in situ trout hearts (Faust et al., 1994; open square, N=8). Workload during the hypoxic period was similar between studies. The ventricular strips used by Gesser (1977) were developing maximum force, but at a contraction rate (0.2 Hz, 12 contractions min–1) much lower than measured in vivo (50–60 beats min–1). By contrast, the power output of the hearts used in Faust et al. (2004) was approx. 1/6th of maximum. Reprinted with permission from the Journal of Experimental Biology.

View larger version (39K): [in a new window]   Fig. 4. Comparison of the ability of preconditioning (5 min ofhypoxic pre-exposure) to protect (A) hypoxia-sensitive (Gamperl et al., 2001) and (B) hypoxia-tolerant (Gamperl et al., 2004) trout hearts from the myocardial dysfunction that follows more prolonged exposure to hypoxia. In A, 5 min of hypoxic pre-exposure completely eliminated the loss of myocardial function that normally followed the `Hypoxia-high workload' protocol. In B, preconditioning with 5 min of hypoxia either did not affect, or increased, the amount of myocardial dysfunction following exposure to `30 min of hypoxia'. Top panels, maximum cardiac output; middle panels, maximum stroke volume; bottom panels, heart rate. Note that the hypoxia-tolerant trout hearts in B required twice the duration of hypoxia (15 vs 30 min), and 6 times the workload, as compared with hypoxia-sensitive hearts (A) to achieve a comparable (15–20%) decrease in post-hypoxic myocardial function. Values were obtained by comparing maximum in situ cardiac function before and after the treatment protocols. All values are means ± S.E.M. (N=7–9). Dissimilar letters indicate a significant difference at P<0.05, as determined by one-way ANOVA. Hypoxia in these experiments was defined as perfusate PO2=5–10 mmHg. Control hearts were only exposed to oxygenated saline.

View larger version (94K): [in a new window]   Fig. 5. Medial section through the alcohol-preserved ventricle of a chinook salmon Oncorhynchus tshawytscha (10 kg). Note location of, and the proportion of, ventricle occupied by the compact (C) and spongy (S) myocardium. Arrows indicate coronary arteries. Original magnification, x5. Reprinted with permission from the American Journal of Physiology (Gamperl et al., 1998).

View larger version (27K): [in a new window]   Fig. 6. Recovery of maximum cardiac output in 10°C in situ cod (Gadus morhua) hearts exposed to oxygenated perfusate only (control), 5 min or 15 min of hypoxia (PO2=5–10 mmHg), or 5 min hypoxia 20 min prior to 15 min of hypoxia (preconditioning). Values are means ± S.E.M. (N=8–9). Dissimilar letters indicate a significant difference at P<0.05 as determined by one-way ANOVA (A. G. Genge and A. K. Gamperl, unpublished).

View larger version (100K): [in a new window]   Fig. 7. Photographs of hearts from (A) an uninfected cod (Gadus morhua) and (B) one that was infected with an X-stage Lernaeocera branchialis. (C) Cross section though the bulbus (i) and connective tissue `capsule' (ii) that had grown around the parasite and allowed for additional blood flow. * and ** indicate the locations of the labeled portions of the parasite's cephalic anchors. (D) Chitinous exoskeleton of the cephalic anchors that were imbedded in the bulbus and capsule. The anchor in the bulbus (**) occluded a significant portion of the bulbus' lumen. Scale bar in D, 1 mm.