It has been hypothesized that blood flow through high grade stenotic arteries may produce conditions in which elastic flow choking may occur. The development of atherosclerotic plaque fracture may be exacerbated by the compressive stresses during collapse. This study explored the effects of pulsatile flow on stenotic flow collapse. Pulsatile flow was produced using a gear pump controlled by a digitized physiologic waveform. Upstream and downstream mean pressures and pulsatile flow rates were measured and digitized. An improved model of arterial stenosis was created using an elastomer with an incremental modulus of elasticity matched to a bovine carotid artery in the relevant range of collapse. Additionally, the model retained a very thick wall in the stenotic region similar to arterial disease. Flow choking was observed for pulsatile pressure drops close to those previously reported for steady flow. The phase difference between flow rate and pressure between upstream and downstream of the stenosis occurred by the compliance of tube and stenosis resistance. For 80% nominal stenosis by diameter and 100+/-30mmHg upstream pressure, collapse occurred for average pulsatile pressure drops of 93mmHg. Pulsatile flow experiments in this model revealed the range of conditions for the flow choking and the paradoxical collapse of the stenosis during systole with expansion during diastole. The stenosis severity was dynamic through the pulse cycle and was significantly greater under flow than the nominal severity. The results indicate that flow choking and stenotic compression may be significant in thick-walled arterial stenoses subjected to pulsatile flow.