Abstract
In order to determine how histamine raises small venous pressure in the dog foreleg, response of pressure during spontaneous blood flow was compared with that during constan blood flow. With spontaneous blood flow, small venous pressure rose in response to both slow and fast rates of infusion of histamine into the brachial artery. Rise of small venous pressure preceded rise of interstitial pressure. Edema appeared whenever small venous pressure exceeded 26 mm Hg for 7 minutes or more. With blood flow held constant, slow rates of infusion failed to either raise small venous pressure or produce edema. Pressure rose and edema appeared despite a constant blood flow rate when the rate of infusion was increased to values which lowered systemic arterial pressure. Pressure increase was unaffected by section of foreleg nerves but was partially abolished by adrenergic blockade. Rapid intravenous infusion during constant blood flow raised small venous pressure much less and this rise was completely abolished by adrenergic blockade. These studies indicate that low rates of infusion into the brachial artery raise small venous pressure by arteriolar dilatation whereas high rates raise this pressure both by arteriolar dilatation and venous constriction. Venous constriction probably results both from a direct action of histamine and indirectly through an adrenal discharge. The study also suggests that elevation of capillary hydrostatic pressure is an adequate explanation for histamine edema.