Temperature Effects on the Responses to Prolonged Submergence in the Turtle Chrysemys picta bellii. I. Blood Acid-Base and Ionic Changes during and following Anoxic Submergence

• Published in: Physiological zoology 1985-11, Vol.58 (6), p.655-669
• Main Authors: Herbert, Christine V., Jackson, Donald C.
• Format: Article
• Language: English
• Subjects: Acidosis; Anoxia; Biological and medical sciences; Blood; Blood plasma; Fundamental and applied biological sciences. Psychology; Ion temperature; Lactates; Plasma temperature; Temperature control; Thermoregulation. Hibernation. Estivation. Ecophysiology and environmental effects; Turtles; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0031-935X
• DOI: 10.1086/physzool.58.6.30156070

Blood acid-base status and plasma ion concentrations and osmolality of freshwater turtles (Chrysemys picta bellii) were measured periodically during and following submergence in N₂-equilibrated water (Po₂ < 5 torr) at 3, 10, 15, and 20 C. Submergence durations that resulted in similar reductions in blood pH or in plasma [HCO₃⁻] at each temperature were 12 h at 20 C, 3 days at 15 C, 10 days at 10 C, and 13 wk at 3 C. At 3 C, 75% of the fall in pH during anoxia was due to metabolic acidosis, but the contribution of respiratory acidosis to the pH drop increased with temperature, being 50% at 10 C, 73% at 15 C, and 73% at 20 C. Plasma strong-ion difference decreased much less during anoxia than had been predicted on the basis of the increase in plasma lactate, owing to compensatory changes in plasma ions, including increased [K⁺], total [Ca⁺⁺], and total [Mg⁺⁺] and decreased [Cl⁻]. The magnitude of these ion changes was directly correlated with the increase in plasma lactate, which in turn was inversely correlated with temperature. Plasma lactate concentrations ranged from 96 mM at 3 C to 19.7 mM at 20 C. Recovery from anoxic acidosis at all temperatures occurred in two stages, a respiratory stage that rapidly restored blood pH and lowered blood PCo2 below control values and a slower ionic stage that corrected plasma lactate and the associated disturbances in other plasma ions. Plasma osmolality increased during anoxia, and the extent of the increase varied inversely with temperature, as did the net increase in measured plasma ions. We conclude that the prolonged tolerance to anoxia at 3 C is not due to specialized mechanisms absent at higher temperatures; rather, slow accumulation of plasma lactate, modest hypercapnia, and effective compensatory ion changes markedly retard the development of acidosis at this temperature.