The roles of oxygen delivery and electrolyte levels in the dehydrational death ofXenopus laevis

Summary

• 1. In order to determine mechanisms which extend desiccation tolerance in terrestrial anurans, a study of the physiological processes failing in dehydrational death was undertaken withXenopus laevis. At various degrees of dehydration, measurements of resting and active metabolic rates, resting and active heart rates, resting arterio-venous blood oxygen contents (a-v differences), and resting whole animal lactate levels were made to assess cardiovascular-respiratory capabilities.X. laevis was also subjected to various osmotic and ionic loads in order to assess the roles which total osmotic pressure and sodium ion may play in dehydrational death and the animals' ability to consume oxygen.

• 2. Maximal oxygen consumption rates ($\dot V_{O_2 }$max) significantly decreased following evaporative water losses of 20 and 30% of initial body weight when compared to values for hydrated toads. Routine metabolic rates were unaffected by dehydration.

• 3. Resting heart rates increased with increasing dehydration, while maximal heart rates declined. There was no difference between resting and active rates at a loss of approximately 25% of original body weight.

• 4. At critical activity point (CAP, the inability to right) there was a significant increase in whole animal lactate, indicating an inability to supply resting metabolic demands aerobically.

• 5. Following dehydrations to CAP, a-v differences in blood oxygen content increased from values in normally hydrated frogs and venous saturation decreased, indicating a limitation in oxygen delivery.

• 6. A generalized decline in aerobic metabolic capabilities measured as$\dot V_{O_2 }$max could be elicited by salt loadingXenopus. Hematocrit was unchanged in these experiments, thus indicating an intrinsic osmotic effect independent of viscosity effects.

• 7. The nonpermeant osmotic concentration at CAP chieved either by sucrose or sodium chloride load was around 440 mosM. This was the same nonpermeant osmotic concentration at CAP in normally dehydrated frogs.

• 8. A critical problem during dehydration inX. laevis appears to be a curtailment of circulatory oxygen delivery capabilities eventually leading to generalized anoxia. The ultimate reason for this debilitation seems tied to a nonpermeant plasma osmotic concentration of around 440 mosM. Increasing viscosity may accentuate this phenomenon but it is not entirely responsible for it.