Abstract
During prolonged experimental submergence, freshwater turtles become anoxic and develop a combined respiratory and non-respiratory acidosis. Anoxia and acidosis are known to depress cardiac function in turtles and other vertebrate species. In vitro studies of ventricular and atrial tissue of turtles indicate that increased extracellular Ca++ concentration can reverse these depressant actions. Intact turtlesutilize this compensatory mechanism during anoxia and other conditions leading to acidosis byincreasing plasma Ca++ concentration. In addition, cardiac cells may release Ca++ from cell organelles to compensate for induced respiratory acidosis. Both mechanisms presumably improve cardiac contractility by elevating the level of sarcoplasmicCa++.
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