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Departments of 1 Biological Sciences and 2 Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6
Studies with mammals and birds clearly
demonstrate that brief preexposure to oxygen deprivation can protect
the myocardium from damage normally associated with a subsequent
prolonged hypoxic/ischemic episode. However, is not known
whether this potent mechanism of myocardial protection, termed
preconditioning, exists in other vertebrates including fishes. In this
study, we used an in situ trout (Oncorhynchus mykiss)
working heart preparation at 10°C to examine whether prior exposure
to 5 min of anoxia (PO2 
5 mmHg) could reduce
or eliminate the myocardial dysfunction that normally follows 15 min of
anoxic exposure. Hearts were exposed either to a control treatment
(oxygenated perfusion) or to one of three anoxic treatments:
1) anoxia with low Pout [15 min of anoxia at an
output pressure (Pout) of 10 cmH2O];
2) anoxia with high Pout [10 min of anoxia at a
Pout of 10 cmH2O, followed by 5 min of anoxia
at Pout = 50 cmH2O]; and 3)
preconditioning [5 min of anoxia at Pout = 10 cmH2O, followed after 20 min of oxygenated perfusion by the
protocol described for the anoxia with high Pout group].
Changes in maximum cardiac function, measured before and after anoxic
exposure, were used to assess myocardial damage. Maximum cardiac
performance of the control group was unaffected by the experimental
protocol, whereas 15 min of anoxia at low Pout decreased
maximum stroke volume (Vs max) by 15% and maximum cardiac
output (
max) by 23%. When the anoxic workload was
increased by raising Pout to 50 cmH2O, these
parameters were decreased further (by 23 and 38%, respectively).
Preconditioning with anoxia completely prevented the reductions in
Vs max and max that were observed in
the anoxia with high Pout group and any anoxia-related
increases in the input pressure (Pin) required to maintain
resting (16 ml · min
1 · kg1).
Myocardial levels of glycogen and lactate were not affected by any of
the experimental treatments; however, lactate efflux was sevenfold
higher in the preconditioned hearts. These data strongly suggest that
1) a preconditioning-like mechanism exists in the rainbow
trout heart, 2) increased anaerobic glycolysis, fueled by
exogenous glucose, was associated with anoxic preconditioning, and
3) preconditioning represents a fundamental mechanism of
cardioprotection that appeared early in the evolution of vertebrates.
myocardium; hypoxia; metabolites; anaerobic glycolysis; cardiac output; Oncorhynchus mykiss; glycogen; lactate
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