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

dc.contributor.authorHanson, Linda M.
dc.contributor.authorBaker, Daniel W.
dc.contributor.authorKuchel, Louise J.
dc.contributor.authorFarrell, Anthony Peter (Tony)
dc.contributor.authorVal, Adalberto Luis
dc.contributor.authorBrauner, Colin John
dc.date.accessioned2020-05-07T14:02:11Z
dc.date.available2020-05-07T14:02:11Z
dc.date.issued2009
dc.description.abstractThe 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.en
dc.identifier.doi10.1242/jeb.022764
dc.identifier.urihttps://repositorio.inpa.gov.br/handle/1/15046
dc.language.isoenpt_BR
dc.publisher.journalJournal of Experimental Biologypt_BR
dc.relation.ispartofVolume 212, Número 9, Pags. 1270-1276pt_BR
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Brazil*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/br/*
dc.subjectCarbon Dioxideen
dc.subjectAdaptationen
dc.subjectAnimalsen
dc.subjectBlooden
dc.subjectCatfishen
dc.subjectHearten
dc.subjectIn Vitro Studyen
dc.subjectPhen
dc.subjectPhysiologyen
dc.subjectAdaptation, Physiologicalen
dc.subjectAnimalen
dc.subjectCarbon Dioxideen
dc.subjectCatfishesen
dc.subjectHearten
dc.subjectHydrogen-ion Concentrationen
dc.subjectAnimalsiaen
dc.subjectLiposarcus Pardalisen
dc.subjectOligacanthorhynchusen
dc.subjectTeleosteien
dc.titleIntrinsic mechanical properties of the perfused armoured catfish heart with special reference to the effects of hypercapnic acidosis on maximum cardiac performanceen
dc.typeArtigopt_BR

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