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Substrate Preference and Metabolic Activity of the Aerobic and the Hypoxic Turtle Heart
Substrate utilization by the isolated aerobic (Po2 500 mm Hg) and hypoxic (Po2 50 mm Hg) turtle (Pseudemys scripta) heart was evaluated by retrograde perfusion. During aerobic perfusion, the heart demonstrated active extraction and oxidation of free fatty acid (FFA) even in the presence of exogenous...
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Published in: | Circulation research 1972-09, Vol.31 (3), p.453-467 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Substrate utilization by the isolated aerobic (Po2 500 mm Hg) and hypoxic (Po2 50 mm Hg) turtle (Pseudemys scripta) heart was evaluated by retrograde perfusion. During aerobic perfusion, the heart demonstrated active extraction and oxidation of free fatty acid (FFA) even in the presence of exogenous glucose. FFA metabolism was similar to that seen in the mammalian heart and was adequate to meet most of the myocardial energy requirements. When hypoxia supervened, FFA utilization did not compete with, but rather enhanced, concomitant carbohydrate metabolism, and glycogenolysis provided sufficient substrate to meet myocardial energy requirements with little change in observed hemodynamic function. During hypoxia, both rat and turtle demonstrated enhanced myocardial esterification of extracted [1C]-palmitate into neutral lipid. Exogenous glucose provided the glycerophosphate skeleton for FFA esterification in the hypoxic rat heart; endogenous glycogen served this function in the turtle myocardium. Extraction of glucose by the turtle heart was limited and changed insignificantly during hypoxia. The rat heart increased glucose uptake five-fold during hypoxia. Glycogen stores in turtle heart were tenfold greater than they were in rat heart, and they provided greater metabolic flexibility and permitted the heart to function adequately under environmental conditions that are lethal to the mammal. |
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ISSN: | 0009-7330 1524-4571 |
DOI: | 10.1161/01.RES.31.3.453 |