Key result
Combined anoxia and acidosis depletes turtle cardiac creatine phosphate by ~86% and drives severe intracellular acidosis.
Why the study?
The resistance of turtle hearts to anoxia and acidosis and their effects on intracellular pH and high-energy phosphates were not well characterized compared to mammalian hearts.
Population
Isolated turtle hearts (Chrysemys picta bellii)
Comparison
4 h anoxia vs 4 h lactic acidosis vs 1.5 h combined anoxia + acidosis vs control
Design
Preclinical experimental study using 31P-NMR spectroscopy
Follow-up
Up to 4 hours of intervention and 2 hours of recovery
Authors
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Turtle myocardial resilience to isolated and combined anoxia-acidosis extends comparative models of cardiac tolerance; leaves open mechanisms relevant to mammalian ischemia.
Turtle hearts demonstrate relative resistance to anoxia and acidosis compared with mammalian hearts, with findings suggesting no direct causal relationship between myocardial CP or ATP levels and cardiac function during anoxia.
Wasser et al. (1990) studied isolated turtle hearts during anoxia and acidosis. Anoxia, lactic acidosis, or combined anoxia and acidosis vs. Control was evaluated on intracellular pH (pHi) and high-energy phosphate levels. Turtle hearts were relatively resistant to anoxia and acidosis, though combined anoxia and acidosis profoundly decreased creatine phosphate to 14% and pHi to 6.56.
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