Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs

1. With pentobarbitone-anaesthetized dogs, the cranial tracheal arteries have been independently perfused on both sides, to measure vascular resistance. Blood pressure and contractions of tracheal muscle were also measured. 2. Capsaicin was injected intravenously to stimulate lung C-fibre receptors. In breathing and in paralysed artificially ventilated dogs it decreased tracheal vascular resistance and blood pressure, and contracted tracheal muscle. The effects were abolished or far smaller after bilateral cervical vagosympathectomy. 3. Veratrine was injected intravenously to stimulate slowly adapting pulmonary stretch receptors and cardiac receptors. In breathing and in artificially ventilated dogs it lowered tracheal vascular resistance and blood pressure, and had variable effects on tracheal muscle tone. The vascular effects were prevented by vagotomy. 4. Veratrine injected into the left atrium caused similar vascular changes to intravenous administration. The changes were prevented by vagotomy. Veratrine causes a tracheal vasodilatation by action on cardiac receptors. 5. Inflation of the lungs in artificially ventilated dogs, to stimulate slowly adapting pulmonary stretch receptors, had no effect on tracheal vascular resistance but decreased blood pressure and tracheal muscle tone, the latter being prevented by vagotomy. 6. Bilateral carotid arterial occlusion, to decrease the discharge in carotid sinus baroreceptors, had no effect on tracheal vascular resistance but increased blood pressure and contracted tracheal muscle, the last two responses being greatly reduced by cutting the sinus nerves. 7. It is concluded that stimulation of lung C-fibre and cardiac receptors causes a reflex tracheal vasodilatation, but that no changes in the tracheal vascular bed occur with stimulation of slowly adapting pulmonary stretch receptors or inhibition of carotid sinus baroreceptors.