Despite widespread use of the Medical Anti-Shock Trousers (MAST) little is known about the exact mechanism by which they increase arterial pressure. It is assumed that an autotransfusion occurs. To examine this question, blood pressure, heart rate, forearm blood flow, cardiac output, and stroke volume were measured in ten healthy adults, supine and during 60 degree headup tilt with MAST garment pressures of 409 and 100 mm Hg. Supine, the garment produced no net 'autotransfusion,' but raised blood pressure (27%) by increasing peripheral resistance (48%) with decreased stroke volume and cardiac output (18%). During headup tilt without the MAST device, venous pooling in the legs decreased stroke volume (52%), cardiac output (30%), and increased total peripheral resistance (40%). Application of the garment during tilt shifted this blood centrally, producing increased stroke volume (52%), cardiac output (30%), and increased total peripheral resistance (40%). Application of the garment during tilt shifted this blood centrally, producing increased stroke volume (14%). In supine normovolemic subjects, the garment raised pressure almost exclusively by increased systemic afterload. Forearm vascular resistance did not change and the increased pressure augmented flow to the arm, i.e., to noncompressed tissue. With increased venous pooling during tilt, the MAST garment acted as a 'G-suit' and caused a central shift of blood volume. These findings could explain: 1) why fluid replacement is not always adequate to maintain pressure when deflating the trousers; 2) why the trousers should not be used if one wishes to avoid increasing afterload (e.g., certain patients with acute myocardial infarction). We conclude that the MAST garment acts as a local, effective, nonpharmacologic vasoconstrictor and should be used when such an effect is clinically appropriate.