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First published online April 17, 2009
Journal of Experimental Biology 212, 1270-1276 (2009)
Published by The Company of Biologists 2009
doi: 10.1242/jeb.022764

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Intrinsic mechanical properties of the perfused armoured catfish heart with special reference to the effects of hypercapnic acidosis on maximum cardiac performance

Linda M. Hanson^1,*, Daniel W. Baker¹, Louise J. Kuchel^1,, Anthony P. Farrell², Adalberto L. Val³ and Colin J. Brauner¹

¹ Department of Zoology, University of British Columbia, 6270 University Boulevard, Vancouver, BC, V6T 1Z4 Canada
² Faculty of Land and Food Systems and Department of Zoology, University of British Columbia, Vancouver, V6T 1Z4 Canada
³ Laboratory of Ecophysiology and Molecular Evolution, Instituto Nacional de Pesquisas da Amazônia, Manaus, Brazil

^* Author for correspondence (e-mail: hanson{at}zoology.ubc.ca)

Accepted 9 February 2009

The armoured catfish, Pterygoplichthys pardalis, is known to be extremely tolerant of environmental hypercarbia (elevated water CO₂ tensions), which occurs in their natural environment. In addition, previous studies have demonstrated that during exposure to hypercarbia, P. pardalis does not exhibit extracellular pH compensation and thus the heart and other organs must continue to function despite a severe extracellular acidosis. We used an in situ perfused heart preparation to determine the effects of an extracellular hypercapnic (elevated CO₂ in the animal) acidosis (1–7.5% CO₂) on heart function, specifically cardiac output, power output, heart rate and stroke volume. The present study is the first to comprehensively examine cardiac function in an acidosis-tolerant teleost. When compared with control conditions, maximum cardiac performance was unaffected at levels of CO₂ as high as 5%, far exceeding the hypercapnic tolerance of other teleosts. Moreover, P. pardalis exhibited only a moderate decrease (35%) in cardiac performance when exposed to 7.5% CO₂, and full cardiac performance was restored in six out of seven hearts upon return to control conditions. Myocardial intracellular pH (pH_i) was protected in situ, as has been found in vivo, and this protection extended to the highest level of CO₂ (7.5%) investigated. Thus, maintained heart function during a hypercapnic acidosis in P. pardalis is probably associated with preferential pH_i regulation of the heart, but ultimately is not sufficient to prevent loss of cardiac function. Our findings suggest the need for further study to elucidate the mechanisms behind this remarkable cardiac hypercapnic tolerance.

Key words: hypercapnia, heart, carbon dioxide, intracellular pH, Pterygoplichthys pardalis, acid–base physiology

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