Effects of vasoconstrictor and vasodilator substances on pulmonary circulation on pulmonary circulation

Abstract

The effects of vaso-constrictor and vaso-dilatator substances on pulmonary circulation are studied experimentally in anaesthetized dogs. Experiments are carried out with simultaneous registration of pressure in the femoral artery, the pulmonary artery and the two auricles. The resistance of the lung to active insufflation and the volume of expired air are also registered, artificial respiration with constant pressure being practiced.

When the animal conserves the normality of its vascular reflexes, the effect of adrenaline is characterized by a phase of pronounced hypotension of proportional intensity and simultaneous to the reflex bradicardia. The latter neutralizes transitorily the effect of vaso-constriction in pulmonary circulation by causing a reduction in the minute output of the right ventricle, and consequently in the repletion of the pulmonary artery. When adrenalinic hypertension diminishes in major circulation, the pulmonary arterial pressure is observed to rise above its level previous to the adrenaline injection. This pressor effect is due to disappearance of reflex bradicardia with subsequent increase of the minute output of the right ventricle, and consequently of pulmonary arterial repletion.

When the same dosis of adrenaline is repeated after alimination of the carotid sinus, after previous section of the vagus or after an atropine injection, the phase of initial or intercalary hypotension is not observed, the pressor effect being always well evident. In this case the rise of pressure is due to the fact that in the absence of reflex bradicardia, the minute output of the right ventricle is maintained or even increased, and' thus the greater repletion of the pulmonary vessels is added to the vasoconstrictor effect of adrenaline on same.

Histamine, as well as acetylcholine generally produces a rise of pulmonary arterial pressure. Observation of the graphics suggests that such an effect may largely depend on the increase of peripheric resistance in pulmonary circulation. However this increase of peripheric resistance is probably not due only to a direct action of histamine on the pulmonary vessels. It may more logically be attributed to extra-vascular effects depending on the contraction of the flat pulmonary muscle or on bronchial constriction, specially when the latter provokes a transitory situation of emphysem, as may be deducted from the registration of expired air volume and of the resistance shown by the lung against active insufflation.

Observation of the effects produced in pulmonary arterial pressure by vaso-constrictor and vaso-dilatator substances employed in these experiments suggests that in the mentioned pressure, the vascular peripheric resistance is a secondary factor. Further that the pressor and depressor effects depend chiefly on the variations of blood volume contained in the pulmonary artery (in relation to the minute output of the right ventricle), and on pulmonary influences extrinsic to the vascular system,

The variations in the minute output of the right ventricle depend chiefly on frequency changes provoked directly or in reflex, by the mentioned substances, and they may also be influenced by modifications of the venous return caused by the direct or reflex action of the drugs on major circulation.