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First published online June 7, 2004
Journal of Experimental Biology 207, 2497-2505 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01055
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Hypoxia tolerance and preconditioning are not additive in the trout (Oncorhynchus mykiss) heart

A. Kurt Gamperl1,*, Heather A. Faust1,{dagger}, Bekah Dougher1 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



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Fig. 1. Protocols used in Experiment 1. Hearts were exposed to one of four treatments: (A) control, (B) 5 min of severe hypoxia, (C) 30 min of severe hypoxia or (D) 5 min of severe hypoxia (preconditioning) followed by 30 min of severe hypoxia. The solid line represents the pressure development of the ventricle as determined by the height of the output pressure (POUT) head, which was set to either a physiologically relevant level of 5.0 kPa, or a sub-physiological level of 1.0 kPa. 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 bold steps mark the maximum cardiac output tests (max), where PIN was raised sequentially from 0.3 kPa to 0.4 kPa, and finally to 0.45 kPa. The shaded rectangles represent periods of severe hypoxia (PO2=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 ml min-1 kg-1, by adjusting PIN as needed.

 


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Fig. 2. Protocols used in Experiment 2. Hearts were exposed to one of four treatments: (A) control, (B) 5 min of severe hypoxia, (C) 30 min of severe hypoxia or (D) 5 min of severe hypoxia (preconditioning) followed by 30 min of severe hypoxia. All other details are described in Fig. 1.

 


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Fig. 3. The effect of pre-exposure to 5 min of severe hypoxia (preconditioning) on (A) resting input pressure (PIN) prior to max1 (1) and max2 (2) and (B) the increase in resting PIN between max2 and max1. *Significant differences (P<0.05), identified using repeated-measures ANOVA. One-way ANOVA did not identify any significant differences between the treatments. Values are means ± S.E.M. (N=7–8 in each group).

 


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Fig. 5. Effect of hypoxic preconditioning (5 min of severe hypoxia) on the recovery of maximum cardiac performance of in situ rainbow trout hearts exposed to 30 min. of severe hypoxia (N=7–8 in each group). (A) Comparison of maximum cardiac performance at max1 and max2. (B) The percentage change in cardiac performance, max2 relative to max1. *Significant difference (P<0.05), as determined using repeated-measures ANOVA. Dissimilar letters represent a significant difference (P<0.05) between treatment groups, as determined using one-way ANOVA. Values are presented as means ± S.E.M.

 


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Fig. 4. Effect of hypoxic preconditioning (5 min of severe hypoxia) on the loss of cardiac output () during a subsequent 30 min hypoxic exposure (N=7–8 in each group): 5 min of hypoxic-preconditioning (filled squares); 30 min of severe hypoxia (filled circles); and 30 min of severe hypoxia following 5 min of hypoxic preconditioning (open squares). Repeated-measures ANOVA indicated that pre-exposure to 5 min of hypoxia did not affect the rate at which fell when hearts were exposed to 30 min of severe hypoxia. Values are means ± S.E.M.

 


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Fig. 6. Effect of 30 min of severe hypoxia, with and without 5 min of hypoxic preconditioning, on in situ maximum cardiac performance (N=7–8 per group). Control (open bars), 5 min hypoxic preconditioning (light gray bars), 30 min severe hypoxia (dark gray bars), 5 min hypoxic preconditioning followed by 30 min of severe hypoxia (black bars). Dissimilar letters represent a significant difference (P<0.05) between treatment groups, as determined using one-way ANOVA. Values are means ± S.E.M.

 





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