The direct effect on pulmonary stretch receptor discharge produced by changing lung carbon dioxide concentration in dogs on cardiopulmonary bypass and its action on breathing.

Abstract

6. In these conditions, the reflex response to C02 could be simulated provided that the pulmonary stretch receptor had an end-expiratory discharge.7. It is suggested that the vagally mediated tachypnoeic response to changes in airway C02 seen in conditions of cardiopulmonary bypass is due to the effect of C02 on the end-expiratory discharge of pulmonary stretch receptors.

A quantitative description of the pattern of breathing during steady‐state CO2 inhalation in man, with special emphasis on expiration

“…The direct desensitizing effect of C02 on the stretch receptor endings may be important for TE in the dog (Bartoli, Cross, Guz, Jain, Noble & Trenchard, 1974;Bradley, Noble & Trenchard, 1976), but what may be the corresponding effect in man is small (Cunningham, Drysdale, Gardner, Jensen, Petersen & Whipp, 1977). It follows that, on the afferent side, a large part of the effect of drive on TE is exerted by some means other than the inhibitory effect of C02 on the pulmonary stretch receptors.…”

Functional characteristics of slowly adapting pulmonary stretch receptors in the turtle (Chrysemys picta).

“…As reported for the dog (Bradley et al 1976) the effects were not linear but were greater over the lower range of CO2 concentrations both during static lung inflations and during pump ventilation. Over a range of CO2 concentrations from 0 to 5%, during pump ventilation, there was an average reduction of 10% of control in peak discharge rate per 10 mmHg increase in PCO2 and 7 % of control in end-expiratory discharge per 10 mmHg increase in PCO2.…”

“…The sensitivity of receptors to static volume inflations was reduced to 9*2 and 6*8 Hz/kPa when animals were ventilated with 5 and 10% CO2 respectively. These values represent 39 and 55% reductions, slightly greater than the 20-40% reductions reported in rabbits, cats and dogs ventilated with 7-9% CO2 in 02 (Mustafa & Purves, 1972;Kunz et al 1976;Bradley et al 1976). …”

“…The time course of the increase in mechanical threshold and decrease in sensitivity of receptors when CO2 was administered during pump ventilation in turtles is similar to mammals (Mustafa & Purves, 1972;Schoener & Frankel, 1972;Bradley et al 1976) as is the time course of recovery when CO2 is removed (Adrian, 1933;Mustafa & Purves, 1972;Bradley et at. 1976;Bartlett & Sant'Ambrogio, 1976).…”

“…The effect of CO2 on pulmonary receptor discharge in the bird is a major, if not dominant factor in the regulation of avian respiration (Kunz & Miller, 1974a, b). Although not a major factor in control of mammalian respiration, the effect of C02 on the discharge of mammalian pulmonary receptors does account for a vagally mediated tachypnoeic response to inhaled CO2 (Mustafa & Purves, 1972;Bartoli et al 1974;Bradley, Noble & Trenchard, 1976).…”