Pulmonary receptors and their role in the control of breathing in turtles
Creators: name: Milsom, William Kenneth
Publisher: name: University of British Columbia
Year: 2010

description: The normal breathing pattern recorded in unanaesthetized, lightly re-strained turtles, Chrysemys picta, consisted of periods of continuous breathing interspersed with periods of breath holding. During each ventilatory period, respiratory frequency and tidal volume were controlled separately and independently of breath length, the total inspiratory interval, the active inspiratory interval and the expiratory interval. Increases in pulmonary minute ventilation during hypercapnia were caused by increases in respiratory frequency due solely to shortening of the intervals of breath holding. The frequency of breathing within each ventilatory period remained constant. There was a large variability in inspiratory and expiratory gas flow rates yet tidal volume was maintained within narrow limits by adjustment of the lengths of the active inspiratory and expiratory intervals. This mechanism was dependent upon lung volume information carried within the vagus nerve. Following vagotomy, changes in minute ventilation due to hypercapnia stemmed primarily from changes in tidal volume while changes in respiratory frequency were markedly reduced. Lung volume information carried within the vagus nerve arose from slowly adapting pulmonary stretch receptors. Single fibre nerve activity from pulmonary receptors was recorded from vagal slips in single-pithed tidally ventilated turtles. The major stimulus of these receptors was the change in lung volume throughout each breathing cycle. The rate and degree of change in transpulmonary pressure were without direct effect on receptor discharge. The functional characteristics of these receptors differed only quantitatively from those recorded in pulmonary stretch receptors of mammals and these differences probably stem from the lower body temperature of the turtle and the location of the receptors in the turtle lung. Most receptors were sensitive to CO₂, several sufficiently sensitive that both tonic and phasic receptor discharge were totally inhibited throughout the ventilatory cycle by 5 to 10% CO₂ in the inspired gas. Pulmonary mechanoreceptors in the frog were also shown to be sensitive to. The acute sensitivity to of a few receptors in turtles and frogs parallels that of the intrapulmonary receptors described-in birds and suggests that a pulmonary receptor with distinct mechano- and chemosensitive properties may represent the functional precursor of the variety of pulmonary receptor types which appear in modern day vertebrates. To examine the role of sensitivity of pulmonary receptors in the overall response of turtles to inhaled CO₂, ventilatory responses of unanaesthetized turtles to changes in the intrapulmonary CO₂ content of a vascularly isolated lung (constant PaCO₂ ) and an intact lung were measured during spontaneous breathing. The isocapnic hyperpnea associated with inhalation of CO₂ by the vascularly isolated lung was small and abolished by vagotomy. It is concluded that both inhibition of pulmonary stretch receptor discharge with increasing levels of FICO₂ and a functional increase in central inspiratory volume threshold contributed significantly to tidal volume increases during hypercapnia. The primary ventilatory response of intact turtles to increasing levels of FICO₂ was an increase in respiratory frequency and this response FICO₂ was greatly reduced when CO₂ was inspired only by the vascularly isolated lung. Thus the ventilatory response of turtles to increasing levels of FICO₂ is primarily dependent upon increased levels of arterial CO₂. The effect of vagotomy in producing apneusis in turtles supports suggestions they lack a pneumotaxic centre. The arrhythmic breathing pattern in turtles with intact vagal nerves, however, bears no similarity to the pattern of breathing in mammals with only the pneumotaxic centre ablated. It is concluded that the vagal input from pulmonary receptors to the respiratory centres in turtles is qualitatively similar to that in mammals yet the differences in central integration of lung volume information in turtles and mammals are not due solely to the absence of a pneumotaxic centre in the turtle. Many of the remaining differences may arise from the lower metabolic demand of turtles but how this affects central integration and respiratory pattern generation is unknown.