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First published online February 6, 2004
Journal of Experimental Biology 207, 1005-1015 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.00824

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All rainbow trout (Oncorhynchus mykiss) are not created equal: intra-specific variation in cardiac hypoxia tolerance

Heather A. Faust^1,*, A. Kurt Gamperl^1, and Kenneth J. Rodnick²

¹ Department of Biology, Portland State University, PO Box 0751, Portland, OR 97207-0751, USA
² Department of Biological Sciences, Idaho State University, Pocatello, ID 82309-8007, USA

View larger version (6K): [in a new window]   Fig. 1. Schematic diagram of the experimental protocol used to confirm that the in situ trout hearts were experiencing severe hypoxia. One group of in situ hearts was perfused with severely hypoxic saline (N=8), while a second group of hearts was perfused with severely hypoxic saline containing 1.5 mmol l–1 of sodium cyanide (NaCN) (N=7). Time intervals are marked in min above the protocol. The solid line represents the end-diastolic pressure developed by the ventricle. POUT was set to a physiologically realistic level of 50 cmH2O. The steps identify the maximum cardiac output tests (MAX), where PIN was raised sequentially from 3 cmH2O to 4 cmH2O, and finally to 4.5 cmH2O. During all periods of oxygenated cardiac perfusion, was maintained at a physiologically resting level of 16–17 ml min–1 kg–1, by adjusting PIN as needed. The shaded rectangle represents the period of severe hypoxia (PO =5–10 mmHg). During hypoxia, PIN was not adjusted and was allowed to fall.

View larger version (20K): [in a new window]   Fig. 2. Experimental protocols used to examine the effect of duration of severe hypoxia (PO =5–10 mmHg) on in situ trout heart function. Hearts were exposed to one of four treatment protocols: (A) control (oxygenated perfusion) (N=7), (B) 10 min (N=7), (C) 20 min (N=7) or (D) 30 min (N=8) of severe hypoxia. In each protocol, the solid line represents the end-diastolic pressure developed by the ventricle, determined by adjusting the height of the output pressure (POUT) head. POUT was set to either a physiologically realistic level of 50 cmH2O, or a sub-physiological level of 10 cmH2O. The arrows () mark the initial cardiac stretch, where input pressure (PIN) was raised to elicit a cardiac output () of 30 ml min–1 kg–1. The steps identify the maximum cardiac output tests (MAX1 and MAX2), where PIN was raised sequentially from 3 cmH2O to 4 cmH2O, and finally to 4.5 cmH2O. The shaded rectangles indicate periods of induced severe hypoxia (PO =5–10 mmHg). During hypoxia, PIN was not adjusted and was allowed to fall. During all periods of oxygenated cardiac perfusion, was maintained at a physiologically resting level of 16–17 ml min–1 kg–1 by adjusting PIN as needed. The small, open squares represent points at which perfusate samples (1 ml) were collected for biochemical analysis.

View larger version (17K): [in a new window]   Fig. 3. Cardiac output () during 15 min of severe hypoxia (filled circles; N=8), and during 15 min of severe hypoxia with 1.5 mmol l–1 of sodium cyanide (NaCN) added to the hypoxic perfusate (open circles; N=7). was averaged over 2 min intervals during severe hypoxia. There was no significant difference in between the treatment groups, at any point during severe hypoxia.

View larger version (17K): [in a new window]   Fig. 4. Decreases in (A) cardiac output and (B) heart rate fH during 10 min (triangles; N=7), 20 min (open circles; N=7) and 30 min (filled circles; N=8) of severe hypoxia. Repeated-measures ANOVA showed that there were no significant differences between the treatments. Data for control fish are not shown because these hearts were not exposed to severe hypoxia, and was maintained at 16–17 ml min–1 kg–1.

View larger version (13K): [in a new window]   Fig. 5. The effect of increasing the duration of severe hypoxia on the input pressure PIN required to maintain a resting cardiac output of 16–17 ml min–1 kg–1. (A) PIN recorded prior to max1 and prior to max2; (B) the change in resting PIN between max1 and max2 (N=6–7 in each group). *Significant difference (P<0.05) identified using repeated-measures ANOVA. One-way ANOVA did not reveal any significant differences in the change in PIN between treatments.

View larger version (38K): [in a new window]   Fig. 6. The effect of increasing the duration of severe hypoxia on maximum cardiac performance of in situ rainbow trout hearts. Hearts were exposed to 0 min (control), or 10 min, 20 min and 30 min of severe hypoxia (N=7–8 in each group). (A) Comparison of maximum cardiac performance between max1 and max2; *significant difference (P<0.05) as determined by repeated-measures ANOVA. (B) The percent change in maximum cardiac performance at max2 relative to max1. Dissimilar letters indicate a significant difference (P<0.05) between treatments, as determined using one-way ANOVA.

View larger version (32K): [in a new window]   Fig. 7. Activity of lactate dehydrogenase (LDH) in baseline (non-experimental) ventricles, and in ventricles exposed to each of the treatments in Experiment 2. Ventricular LDH values are means + S.E.M., where 1 unit = conversion of 1 µmol substrate to product per min. There were no significant differences in average LDH activities between any of these groups (P<0.05), as determined using one-way ANOVA (N=4–7 in each group).

View larger version (16K): [in a new window]   Fig. 8. Recovery of cardiac function following 30 min of severe hypoxia, measured as the percent recovery of maximum force by ventricular strips [Gesser, 1977; open circles, rainbow trout (N=5) and filled circles, carp (N=5)], or as the percent recovery of MAX in the present study (open square, N=8). The 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, whereas the power output of the hearts used in the study was approx. one sixth of maximum.