Diminished poststenotic pressure and flow accompanied experimental application of multiple subcritical arterial stenoses in series. Effects of additional stenoses, causing equivalent constrictions, were cumulative in a nonlinear fashion. Seven-hundred-twenty measurements were performed using 10 cm ileofemoral canine arterial segments in vitro and in vivo with pulsatile and nonpulsatile blood flow. Pressures and flow volumes utilized for testing were within normal physiologic ranges. Data analysis included correlations of experimental observations with predictions generated from a theoretic hydraulic model. Kinetic energy losses with multiple subcritical stenoses were associated with decreased pressure and flow. Poststenotic pressure decreased as much as 51% in some experiments. Diminutions in flow paralleled pressure changes. Measured pressure changes were nonlinear and followed mathematic predictions of appreciable but lesser effects of added stenoses. Hemodynamic alterations of magnitudes documented in this study assume clinical importance. The assumption that a solitary critical stenosis must exist before significant hemodynamic changes occur is no longer tenable.