Abstract
The effect of a large dose of epinephrine in blood was studied in dogs. Pulmonary edema resulted both in the experiments in which injections were made into the carotid artery and in those with intravenous injections. Left ventricular systolic pressures rose more with intravenous than with intracarotid infusions. Left ventricular end-diastolic pressures rose dramatically and rapidly but less with intravenous infusion. There was an increase of the dp/dt peak and ventricular dilatation in both types. Cardiac denervation followed by intracarotid infusion prevented or decreased pulmonary edema in 4 out of 8 experiments.
It is concluded that the rise of left ventricular end-diastolic pressure is a primary factor for the increased pulmonary capillary pressure causing edema. This rise seems to be caused by adrenergic action and efferent sympathetic stimuli affecting both ventricular compliance and peripheral vasoconstriction rather than by myocardial failure in the usual sense.
