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Control of cardiovascular function during prolonged anoxia exposure in the freshwater turtle (Trachemys scripta)

University of British Columbia

Unlike the majority of vertebrates, the freshwater turtle (Trachemys scripta) can survive anoxia for hours at warm acclimation temperatures and weeks at cold acclimation temperatures. During anoxia exposure, the turtle heart continues its role in internal convection, but systemic cardiac output and systemic cardiac power output are massively reduced, primarily due to a decreased heart rate (ƒH). Therefore, control of ƒH is critical to cardiac energy management during anoxia. This thesis investigated what extrinsic, autocrine/paracrine and intrinsic mechanisms control the cardiovascular system of anoxic freshwater turtles. Cardiac control was examined at the level of the whole animal, organ (isolated heart chambers), and cell (isolated cardiac myocytes). A 2 x 2 exposure design allowed comparisons between 21°C- and 5°C-acclimated turtles under normoxia and anoxia. For warm-acclimated turtles, I discovered a re-setting of intrinsic ƒH that accounts for up to 57% of the anoxic bradycardia, which, when combined with cholinergic cardiac inhibition (previously known), fully explains the depression of ƒH with anoxia. Interestingly, prolongation of ventricular action potential duration (APD) by 47% with anoxia was proportional to the reduction in intrinsic ƒH. My thesis also revealed how cold acclimation prepared cardiac muscle for winter anoxic conditions. Cold temperature decreased intrinsic ƒH, prolonged cardiac APDs and reduced the chronotropic sensitivity to extracellular anoxia and acidosis. Also, the decreased peak densities of ventricular I[sub Na] and I[sub Ca] and conductance of i[sub KI] observed in 5°C-acclimated turtle hearts compared with 21°C-acclimated turtle hearts could serve to conserve the ATP cost of ion pumping. When cold-acclimated turtles were exposed to anoxia, during which cholinergic cardiovascular control is blunted, my thesis discovered that a re-setting of intrinsic ƒH accounts for up to 66% of the anoxic bradycardia. However, contrary to 21°C, there was no prolongation of cardiac APDs. No evidence was found for either α-adrenergic or adenosinergic cardiac inhibition in cold-acclimated anoxic turtles, yet their reduction of in vivo cardiac activity correlated with alterations in myocardial high-energy phosphate metabolism, intracellular pH and free energy of ATP hydrolysis. These novel insights point to the importance of future studies on pacemaker currents and cardiac refractoriness.

Text

2011-02-10

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http://hdl.handle.net/2429/31162

Zoology

University of British Columbia

Graduate