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
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

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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 l1 K+, (3) 7.5 mmol
l1 K+, (4) control (recovery) and (5) 7.5 mmol
l1 K+ with 500 nmol l1
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.
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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 l1 K+, pH 7.5,
(3) control (recovery), (4) 5.0 mmol l1 K+ and pH
7.5 with 500 nmol l1 adrenaline (AD), and (5) 7.5 mmol
l1 K+ and pH 7.5 with 500 nmol
l1 AD. Values from series I are presented for comparison
purposes (see Fig. 1). One-way
ANOVA and a HolmSidak multiple comparisons test were used to compare
treatment means. *Significant difference from control; 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
l1 K+ and 5 nmol l1 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.
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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 HolmSidak 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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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 l1), acidotic (pH 7.5) perfusate with both tonic (5
nmol l1) and maximal (500 nmol l1)
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 HolmSidak 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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© The Company of Biologists Ltd 2006