Intravenous injection of epinephrine into the dog produces an increase in fibrinolytic activity of plasma euglobulins. This increase appears to be unrelated to the following epinephrine-induced effects: splenic contraction, stimulation of the lymph circulation, increase in blood glucose, lactic acid, or free fatty acids. A specific involvement of either alpha or beta adrenotropic receptors is ruled out since norepinephrine and isopropylnorepinephrine are equally effective in enhancing fibrinolysis. Intravenous injection of each of a number of vasoactive drugs with different modes of action, and with either hypertensive or hypotensive properties, induces an increase in fibrinolytic activity. Hence, it appears that there is a direct relationship between appearance of increased fibrinolytic activity and vasoactive changes. For all the drugs tested except methoxamine, the maximal fibrinolytic effect is present 5 min after the injection and in general the fibrinolytic activity returns to the preinjection level within 30 min. Repeated injections of a powerful inducer of increased fibrinolytic activity, such as histamine, results in a progressive decrease of the fibrinolytic response.

Venous occlusion for 10 min, by a sphygmomanometer cuff applied above the elbow and maintained at a pressure midway between systolic and diastolic pressure, increases the fibrinolytic activity of the blood within the occluded part of the arm. In six normal human subjects the magnitude of this increase was compared with changes in blood cellular elements, plasma protein concentration, plasma antifibrinolytic activity, and plasma levels of glutamic-oxalacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT). The increase in fibrinolytic activity of the euglobulin fraction of the plasma was 3–20 times larger than the increase in plasma protein concentration and 8–24 times larger than the increase in hematocrit. Venous occlusion produced a rise in antiplasmin and antiurokinase activity of the plasma. The level of GOT in the plasma rose significantly more than the plasma protein concentration. These observations tend to indicate that the activation of fibrinolysis during venous occlusion is brought about by the release of intracellular enzyme(s). fibrinolytic activity of blood; euglobulins; antiplasmin; antiurokinase Submitted on May 31, 1963

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Summary1. Blood fibrinolytic activity and urokinase excretion were studied in a group of young healthy male subjects before and after intravenous injection of nicotinic acid. Although each of the subjects had a marked increase in blood fibrinolytic activity after injection of nicotinic acid, there was no significant change in urokinase excretion.2. These data do not support the theory that urokinase is filtered blood activator of plasminogen. It is suggested that release of urokinase into urine is primarily dependent on the time of contact between urine and walls of collecting ducts and other parts of the urine conducting system.