Ischemia leading to heart attacks and strokes is the major cause of deaths in the world. This report explores the possibility that intracellular material from ruptured endothelial cells is partially responsible for the heterogeneous core-and-shell blood clot architecture, typically observed using intravital microscopy. As evidence, we present a fluid dynamic argument that platelet agonists emanating from the injury cannot activate platelets in the thrombus core, given that they would have to travel against flow of blood escaping into the extravascular. Furthermore, we demonstrate visual evidence that the core material appears to be continuous and originating from the damaged endothelium. Finally, we present a mechanism, illustrating the steps of platelet recruitment into the thrombus and sealing of the injury. If correct, the model presented herein will be beneficial to the understanding and treatment of heart attacks, strokes and hemophilia.
All Science Journal Classification (ASJC) codes
- General Medicine
- Endothelial cells
- Platelet activation