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Title: Intrinsic mechanical properties of the perfused armoured catfish heart with special reference to the effects of hypercapnic acidosis on maximum cardiac performance
Authors: Hanson, Linda M.
Baker, Daniel W.
Kuchel, Louise J.
Farrell, Anthony Peter (Tony)
Val, Adalberto Luis
Brauner, Colin John
Keywords: Carbon Dioxide
In Vitro Study
Adaptation, Physiological
Carbon Dioxide
Hydrogen-ion Concentration
Liposarcus Pardalis
Issue Date: 2009
metadata.dc.publisher.journal: Journal of Experimental Biology
metadata.dc.relation.ispartof: Volume 212, Número 9, Pags. 1270-1276
Abstract: 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 situperfused 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 (pHi) 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 pHi 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.
metadata.dc.identifier.doi: 10.1242/jeb.022764
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