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First published online June 15, 2006
Journal of Experimental Biology 209, 2442-2451 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02237
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The role of adrenergic stimulation in maintaining maximum cardiac performance in rainbow trout (Oncorhynchus mykiss) during hypoxia, hyperkalemia and acidosis at 10°C

Linda M. Hanson1,*, Shannon Obradovich2, Janet Mouniargi3 and Anthony P. Farrell4

1 Department of Zoology, University of British Columbia, 6270 University Blvd., Vancouver, BC V6T 1Z4, Canada
2 Zoophysiology, Gothenburg University, Gothenberg, Sweden
3 Biological Sciences, Simon Fraser University, Burnaby, BC V5A 1S6, Canada
4 Faculty of Land and Food Systems and Department of Zoology, University of British Columbia, Vancouver, BC V6T 1Z4, Canada


Figure 1
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Fig. 1. The effects of hyperkalemia on maximum cardiac output (A) and maximum cardiac power output (B) of perfused rainbow trout hearts at 10°C, pH 7.9. Values are reported as mean ± s.e.m. Individual hearts (N=9) were exposed to the following sequence of perfusates: (1) control (normoxia), (2) 5 mmol l–1 K+, (3) 7.5 mmol l–1 K+, (4) control (recovery) and (5) 7.5 mmol l–1 K+ with 500 nmol l–1 adrenaline (AD). Repeated measures one-way ANOVA and a Holm-Sidak multiple comparisons test were used to compare treatment means. Different letters denote significant differences at P=0.05.

 

Figure 2
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Fig. 2. The effects of hyperkalemia and acidosis (pH 7.5) on maximum cardiac output (A) and maximum cardiac power output (B) of perfused rainbow trout hearts at 10°C. Values are reported as mean ± s.e.m. Individual hearts (N=8) were exposed to the following sequence of perfusates: (1) control (normoxia), (2) 5.0 mmol l–1 K+, pH 7.5, (3) control (recovery), (4) 5.0 mmol l–1 K+ and pH 7.5 with 500 nmol l–1 adrenaline (AD), and (5) 7.5 mmol l–1 K+ and pH 7.5 with 500 nmol l–1 AD. Values from series I are presented for comparison purposes (see Fig. 1). One-way ANOVA and a Holm–Sidak multiple comparisons test were used to compare treatment means. *Significant difference from control; {ddagger}a significant difference from pH 7.9 at that particular level of hyperkalemia, P=0.05. Three preliminary preparations were exposed to 7.5 mmol l–1 K+ and 5 nmol l–1 AD at a pH of 7.5 directly after the first normoxia step. However, this exposure resulted in an almost immediate decrease in cardiac output leading to a rapid (<5 min), irrecoverable cardiac collapse.

 

Figure 3
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Fig. 3. The maximum cardiac output (A) and maximum cardiac power output (B) of perfused rainbow trout hearts at 10°C under hypoxic perfusate. The grey line indicates the level of recovery during a subsequent exposure to normoxic conditions. Individual groups of hearts were exposed to specific hypoxia levels as indicated on the x-axis. Results shown are from two different series of experiments, as indicated by the separate (and discontinuous) line segments; however, experimental protocols were identical up until this point. The number of hearts used for each experiment was in series III: 12.6 kPa (N=6), 10 kPa (N=10), 6.7 kPa (N=6), and in series IV: 5.0 kPa (N=7), 3.3 kPa (N=8), 2.7 kPa (N=5). Values are reported as percentage change from an original assessment under normoxic conditions. One-way repeated-measures ANOVA and Holm–Sidak multiple comparisons tests were used to compare treatment means and each heart acted as its own control. Values shown are means ± s.e.m. *Significant difference from normoxia (P=0.05).

 

Figure 4
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Fig. 4. The change in maximum cardiac output (A) and maximum cardiac power output (B) of perfused rainbow trout hearts at 10°C under hypoxic, hyperkalemic (5 mmol l–1), acidotic (pH 7.5) perfusate with both tonic (5 nmol l–1) and maximal (500 nmol l–1) adrenergic stimulation. Individual groups of hearts were exposed to specific hypoxia levels as indicated on the x-axis, and results are shown from several series of experiments, each indicated as a separate line segment. The series were as follows. Series III: 12.6 kPa (N=6), 10 kPa (N=10), 6.7 kPa (N=6), series IV: 5.0 kPa (N=7), 3.3 kPa (N=8), 2.7 kPa (N=5), and series V: 2.7 kPa (N=6), 2.0 kPa (N=6) and 1.3 kPa (N=4). Values are reported as percent change from an original assessment under normoxic conditions. One-way repeated-measures ANOVA and Holm–Sidak multiple comparisons tests were used to compare treatment means and each heart acted as its own control. Values shown are means ± s.e.m. *Significant difference from normoxia (P=0.05).

 





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