Prolongation in bond lifetime favors spontaneous platelet–VWF interactions. (A-B) Accumulation (A) and translocation velocities (WSR of 1,600 s⁻¹) (B) of human platelets on surface-immobilized plasma VWF^R1326H, VWF^{I1309V, R1326H}, or human VWF at the indicated WSRs. Data are representative of 3 separate experiments performed in duplicate. (C-D) Tail bleeding times (C) and mouse platelet-mediated thrombus formation (D) for WT and mutant VWF-A1 mice pre- and 20 minutes postadministration of human platelets. Platelet-vessel wall interactions were visualized through a ×20 water-immersion objective using a Zeiss Axiotech Vario microscope equipped with a Yokogawa CSU-22 spinning disk confocal scanner, iXon EM camera, and 561 nm laser line. (E) Representative VWF multimer gel of plasma obtained from mutant mice before and 20 minutes after the administration of human platelets. Numbers 1 and 2 denote mice possessing plasma VWF^R1326H or VWF^{I1309V, R1326H}, respectively. (F) Representative tracing of light transmitted aggregometry of human platelets resuspended in plasma obtained from VWF^R1326H or VWF^{I1309V, R1326H} mice. MAb 6D1 is a function blocking antibody to human GPIbα. Data are the mean ± SD. **P < .0001 as compared with VWF^R1326H mice. ns, not significant (P > .05) by unpaired Student t test.