THE PRODUCTION OF SHOCK BY CALLICREIN

Abstract

The intraven. adm. of 200 units of callicrein (60 mg.) to dogs caused irreversible shock and death, usually in 4-7.5 hrs. The mean arterial blood pressure fell precipitously during callicrein adm., partially recovered, and later failed gradually until death. The pulse increased to 200-240 beats/min. The cardiac output was decreased rapidly and to very low values; the O2 consumption was changed similarly to a lesser degree. At autopsy there was a contracted spleen, engorged mesenteric vessels, hyperemic intestinal veins and infiltration of blood into the lumen of the intestines. Callicrein caused a hemoconc. of 10-20 points in normal dogs and only 1-8 points in splenec-tomized dogs. About 30% of both the plasma and red cells were lost from the circulating blood. The arterial blood remained normally oxygenated after callicrein, but the venous blood became progressively unsaturated until death resulted from respiratory failure. An intense acidosis developed; the blood pH fell below 7, and the fixed acid increased 15-30 m. eq./liter. The prep. of callicrein used increased the blood glucose, N.P.N., creatine, and inorganic phosphate. A marked initial leucopenia was followed by a leucocytosis. Callicrein could not be detected in an active form in the blood after the adm. of a lethal dose.