The effects of bilateral vagotomy on pulmonary ventilation, O2 consumption, and heart rate were determined for the water snake, Nerodia sipedon, breathing room air at 15, 25, and 30 degrees C and breathing 5.2% CO2 in air at 25 degrees C. At all body temperatures, vagotomy resulted in a four- to sevenfold increase in tidal volume in snakes breathing room air. At the same time, ventilatory frequency decreased such that pulmonary ventilation was unchanged after vagotomy. Heart rate increased approximately 1.5 times after vagotomy, but O2 uptake was unchanged. The air convection requirement decreased similarly with increasing body temperature in both intact and vagotomized snakes. Arterial pH values were similar to those of intact snakes measured in a previous study and decreased by -0.013 U/degrees C. Since this occurs despite elimination of peripheral chemoreceptor input, it is suggested that the temperature compensation is a centrally controlled process. In intact snakes, breathing CO2 resulted in a fourfold increase in ventilation. Elimination of peripheral receptor input by vagotomy resulted in a loss of this ventilatory response to CO2 breathing. This means that peripheral receptors are required for a response to changes in arterial CO2 partial pressure and pH. Snakes thus differ from turtles and mammals in that central chemoreceptors alone are unable to produce the ventilatory response to inspired CO2.
- Copyright © 1984 the American Physiological Society