Various types of lesions in small and large mouse and human vessels result in high shear rates and elongational flows.
The relative hydrodynamic resistance of the vessel and wound explains a decrease in shear rate with increase in injury size.
Blood flow is a major regulator of hemostasis and arterial thrombosis. The current view is that low and intermediate flows occur in intact healthy vessels, while high shear levels (>2,000 s-1) are reached in stenosed arteries, notably during thrombosis. To date, the shear rates occurring at the edge of a lesion in an otherwise healthy vessel are nevertheless unknown. The aim of this work was to measure the shear rates prevailing in wounds in a context relevant to hemostasis. Three models of vessel puncture and transection were developed and characterized for a study which was implemented in mice and humans. Doppler probe measurements supplemented by a computational model revealed that shear rates at the edge of a wound reached high values, with medians of 22,000 s-1, 25,000 s-1 and 7,000 s-1 after puncture of the murine carotid artery, aorta or saphenous vein, respectively. Similar shear levels were observed after transection of the mouse spermatic artery. These results were confirmed in a human venous puncture model, where shear rates in a catheter implanted in the cubital vein reached 2,000-27,000 s-1. In all models, the high shear conditions were accompanied by elevated levels of elongational flow exceeding 1,000 s-1. In the puncture model, the shear rates decreased steeply with increasing injury size. This phenomenon could be explained by the low hydrodynamic resistance of the injuries as compared to that of the downstream vessel network. These findings show that high shear rates are relevant to hemostasis and not exclusive to arterial thrombosis.