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Towards a molecular explanation of the high performance of the tuna heart
Affiliation:1. Division of Oral and Maxillofacial Pathology, School of Dentistry, University of Minnesota, Minneapolis, MN, USA;2. Cytogenetics Research Core Laboratory, Medical Genome Facility, Mayo Clinic, Rochester, MN, USA;3. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA;1. Center of Marine Sciences, University of Algarve, Ed. 7, Campus of Gambelas, 8005-139 Faro, Portugal;2. Department of Biology, Faculty of Sciences, University of Abdelmalek Essaâdi, Tetouan 93000, Morocco;3. Department of Pharmaceutical Chemistry, Institute of Pharmaceutical Sciences, University of Graz, Austria;4. Department of Biochemistry and Physiology, School of Pharmacy and Food Sciences, University of Barcelona, Joan XXIII, Barcelona, Spain;1. Centre of Excellence for Nutrition, North-West University, Potchefstroom, South Africa 11 Hoffman Street, Potchefstroom; Private Bag X6001, Potchefstroom, 2520, South Africa;2. Hypertension in Africa Research Team (HART), North-West University, Potchefstroom, South Africa;3. Medical Research Council Research Unit for Hypertension and Cardiovascular Disease, North-West University, Potchefstroom, South Africa;4. Chronic Disease Initiative for Africa (CDIA), Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa Barnard Fuller Building, Anzio Road, Observatory, Cape Town, 7935, South Africa
Abstract:The tuna heart is capable of sustaining cardiac outputs that are high relative to other active teleost species. The question as to whether there are known molecular mechanisms to explain this phenomenon is examined. Unfortunately, the evidence at present is scant but the paper attempts to put existing knowledge into a contextual framework. It is known that the high cardiac outputs in tuna are due to the maximum heart rates that are high relative to other active teleost species. While the normalized stroke volume (ml/kg body weight) in tuna is in the same range as that of trout several important points are worth noting. The stroke volume in the tuna heart is generated in the face of an afterload that is two-fold higher (due to high ventral aortic pressure) than that observed in the trout or other teleosts. Since the stroke volume is predicated on the strength of ventricular contraction, the question then arises as to whether this is a consequence of factors intrinsic or extrinsic to the design of the cardiomyocytes that make up the myocardium. Two important extrinsic factors must be noted: the substantially higher normal operating temperatures and the apparent cardiac hyperplasia in the tuna. While the merit of these factors is discussed, the paper focuses on intrinsic factors. There is very little that has been determined to date that would indicate substantive changes in the design of the myocyte in the tuna heart compared to that of trout. Are these extrinsic factors alone then sufficient to account for the impressive cardiac output capabilities in the tuna?
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