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First published online January 17, 2007
Journal of Experimental Biology 210, 421-431 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.02653
Effects of extracellular changes on spontaneous heart rate of normoxia- and anoxia-acclimated turtles (Trachemys scripta)
1 Department of Zoology, University of British Columbia, Vancouver, BC, V6T
1Z4, Canada
2 Faculty of Land and Food Systems and Department of Zoology, University of
British Columbia, Vancouver, BC, V6T 1Z4, Canada
* Author for correspondence (e-mail: jstecyk{at}interchange.ubc.ca)
Accepted 13 November 2006
Heart rate (fH) of the anoxia-tolerant freshwater
turtle (Trachemys scripta) during prolonged anoxia exposure is 2.5-
to 5-times lower than the normoxic rate, but whether alterations in blood
composition that accompany prolonged anoxia contribute to this bradycardia is
unknown. We examined how temperature acclimation, oxygen deprivation,
acidosis, hyperkalemia, hypercalcemia and adrenaline affect chronotropy in the
turtle myocardium. We monitored spontaneous contraction rates of right-atrial
preparations obtained from 21°C- and 5°C-acclimated turtles that had
been exposed to either normoxia or anoxia (6 h at 21°C; 2 weeks at
5°C). Sequential exposures to saline solutions were designed to mimic, in
a step-wise manner, the shift from a normoxic to anoxic extracellular
condition (for normoxia-acclimated preparations) or the reverse (for
anoxia-acclimated preparations). Our results clearly show that prolonged
anoxia exposure re-sets the intrinsic fH of turtles at
both temperatures, with reductions in intrinsic fH in the
range of 25%–53% compared with normoxia. This intrinsic change would
contribute to the bradycardia observed with prolonged anoxia. Further, we
found negative chronotropic effects of extracellular anoxia, acidosis and
hyperkalemia, and positive chronotropic effects of hypercalcemia and
adrenaline. The exact nature of these extracellular effects depended, however,
on the acclimation temperature and the prior exposure of the animal to anoxia.
With normoxia-acclimated preparations at 21°C, combined anoxia and
acidosis (pH reduced from 
7.8 to 7.2) significantly reduced
spontaneous fH by 22% and subsequent exposure to
hyperkalemia (3.5 mmol l–1K+) further decreased
fH. These negative chronotropic effects were ameliorated
by increasing the adrenaline concentration from the tonic level of 1 nmol
l–1 to 60 nmol l–1. However, in
anoxia-acclimated preparations at 21°C, anoxia alone inhibited
fH (by 30%). This negative chronotropic effect was
counteracted by both hypercalcemia (6 mmol l–1
Ca2+) and adrenaline (60 nmol l–1). At 5°C,
only the combination of anoxia, acidosis (pH reduced from 8.0 to
7.5) and hyperkalemia (3.5 mmol l–1 K+)
significantly reduced spontaneous fH (by 23%) with
preparations from normoxia-acclimated turtles. This negative chronotropic
effect was fully reversed by hypercalcemia (10 mmol l–1
Ca2+). By contrast, spontaneous fH of
anoxia-acclimated preparations at 5°C was not affected by any of the
extracellular changes. We conclude that prior temperature and anoxia
experiences are central to determining fH during prolonged
anoxia in Trachemys scripta both as a result of the re-setting of
pacemaker rhythm and through the potential influence of extracellular
changes.
Key words: acidosis, adrenaline, anoxia, calcium, cardiovascular, intrinsic heart rate, potassium, red-eared slider, temperature, Trachemys scripta, turtle
This article has been cited by other articles:
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  J. A. W. Stecyk, V. Paajanen, A. P. Farrell, and M. Vornanen Effect of temperature and prolonged anoxia exposure on electrophysiological properties of the turtle (Trachemys scripta) heart Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R421 - R437. [Abstract] [Full Text] [PDF]
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