Key result
Combined anoxia, acidosis, and hyperkalemia severely disrupt ventricular but not atrial function in anoxic turtles.
Why the study?
It was unclear under what extracellular conditions an inability of the ventricle to contract in coordination with the pacemaker limits cardiac pumping rate during anoxia.
Population
Ventricular and atrial strips from 21 °C- to 5 °C-acclimated turtles (Trachemys scripta)
Comparison
Various extracellular conditions across normoxia vs anoxia exposure (16 h at 21 °C; 12 days at 5 °C)
Design
Preclinical comparative ex vivo tissue study
Authors
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May constrain ventricular output in anoxic turtles; leaves open relevance to mammalian ischemia or clinical cardioprotection.
In cold-acclimated turtles, the ventricle could limit cardiac pumping rate during prolonged anoxic submergence if hypercalcemia and adrenergic stimulation are insufficient to counteract the negative effects of anoxia, acidosis, and hyperkalemia.
Garner et al. (2022) studied Anoxia exposure. Combined extracellular anoxia, acidosis, and hyperkalemia (AAK) vs. Normoxia and other extracellular conditions was evaluated on Intrinsic contractile properties of isometrically-contracting ventricular and atrial strips. Combined extracellular anoxia, acidosis, and hyperkalemia severely disrupted ventricular, but not atrial, excitability and contractibility in 5 °C anoxic turtles.
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