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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 |
Aparece nas coleções: | Artigos |
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