Use este identificador para citar ou linkar para este item: https://repositorio.inpa.gov.br/handle/1/19000
Título: Mitochondrial KATP channels and sarcoplasmic reticulum influence cardiac force development under anoxia in the Amazonian armored catfish Liposarcus pardalis
Autor: MacCormack, Tyson James
Treberg, Jason R.
Val, Vera Maria Fonseca Almeida e
Val, Adalberto Luis
Driedzic, William Robert
Palavras-chave: 5 Hydroxydecanoic Acid
Adenosine Triphosphate
Ryanodine
Anaerobic Capacity
Animals Experiment
Animals Tissue
Anoxia
Catfish
Controlled Study
Heart Mitochondrion
Heart Muscle Contractile Force
Heart Muscle Contracture
Heart Muscle Potential
Heart Protection
Mammal
Nonhuman
Sarcoplasmic Reticulum
Tissue Oxygenation
Animalsia
Catfish
Liposarcus
Liposarcus Pardalis
Loricariidae
Mammalia
Oligacanthorhynchus
Data do documento: 2003
Revista: Comparative Biochemistry and Physiology - A Molecular and Integrative Physiology
É parte de: Volume 134, Número 2, Pags. 441-448
Abstract: The contribution of alterations in mitochondrial KATP channel activity and the sarcoplasmic reticulum (SR) to anaerobic cardiac function in the anoxia tolerant armored catfish Liposarcus pardalis were assessed. KATP channels contribute to hypoxic cardioprotection in mammals, but little is known of their action in more hypoxia tolerant animals. Anoxia resulted in a decrease in force in isometrically contracting ventricle strips to approximately 40% of the pre-anoxic level. This was maintained for at least 2 h. Upon reoxygenation, hearts recovered to the same level as control preparations. Treatment with 5-hydroxydecanoic acid (5HD), a specific mitochondrial KATP blocker significantly increased force in preparations during anoxia and caused hypercontracture at reoxygenation. Ryanodine, a specific inhibitor of SR function, significantly increased force loss in ventricle preparations under anoxia. Results show that mitochondrial KATP channel activity and SR function are important in anaerobic and post-anaerobic contractility in armored catfish heart. © 2002 Elsevier Science Inc. All rights reserved.
DOI: 10.1016/S1095-6433(02)00315-X
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