Abstract
The effect of chemoreceptor stimulation on the pulmonary veins was studied in dogs thoracotomized, artificially respirated, and pretreated with atropine. Pulmonary arterial, pulmonary venous, and left atrial pressures, and pulmonary flow were measured. Nicotine, 5-15 [mu]g/kg, was injected into the ascending aorta near the aortic body chemoreceptors. One to 3 seconds after the injection a rise in the pulmonary arterial and pulmonary venous pressures was observed, while the left atrial pressure and pulmonary flow did not change significantly. The calculated pulmonary venous resistance at rest was 0.057 mm Hg/ml per min and it rose to 0.096 mm Hg/ml per min, a value significantly higher than the control value. This rise paralleled the rise in the pulmonary arterio-capillary resistance (increase from 0.235 to 0.283 mm Hg/ml per min). By selective inactivation of the aortic body and the carotid bodies the sensory receptors for the pulmonary venoconstriction were localized in the aortic body chemoreceptors; no similar effect could be elicited from stimulation of the carotid body chemoreceptors. As sympathetic blockade by guanethidine abolished the response, the efferent arm of the reflex seems to be the pulmonary sympathetic fibers.