Pulmonary Reflexes in Pulmonary Edema?

Abstract

The mechanism of pulmonary edema caused by stimulation of the central nervous system was studied in 33 dogs. Stimulation was obtained by the intracisternal injection of veratrine, or of air or saline under high pressure, or by electric stimulation of the hypothalamus. Pressure changes in the pulmonary artery, left atrium and left ventricle were recorded by means of three catheters introduced through the right external jugular vein and the left femoral artery. Experiments were performed with closed or open chest, and following ligation of the thoracic aorta and inferior cava. Lung opacity was studied as a means to estimate the blood content of this organ. Data obtained in closed-chest experiments suggest that a blood shift from the systemic to the pulmonary circulation may be a factor in veratrine-induced pulmonary edema. This was confirmed by the observation that, following mechanical exclusion of the systemic circulation, no pulmonary edema occurred while the changes of left ventricular pressure were minimal and inconstant. In these animals, pulmonary artery pressure still rose indicating vasoconstriction while an increase of lung opacity suggested that the vasoconstriction was greater in the pulmonary veins than in the arteries. Injection of air or saline under high pressure into the cisterna magna and faradic stimulation of the hypothalamus caused pulmonary hypertension, even after exclusion of the systemic circulation. In these experiments, a decreased lung opacity suggested that the pulmonary constriction was greater on the arterial than on the venous side. These findings are offered as evidence that the caliber of the pulmonary vessels may be influenced by central nervous system stimulation, an additional element to be considered in the mechanism of pulmonary edema.