ArticleBiophysical journal2012
The physical foundation of vasoocclusion in sickle cell disease.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Allosteric control of hemoglobin S fiber formation by oxygen and its relation to the pathophysiology of sickle cell disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular insights into the irreversible mechanical behavior of sickle hemoglobin.Journal of biomolecular structure & dynamics · 2019Article
- Novel in vivo and in vitro techniques to image and model the cerebral vasculature in sickle cell disease.Blood cells, molecules & diseases · 2017Review
- Biomechanics and biorheology of red blood cells in sickle cell anemia.Journal of biomechanics · 2017Review
- Ratchets, red cells, and metastability.Biophysical reviews · 2013Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathology of sickle cell disease arises from the occlusion of small blood vessels because of polymerization of the sickle hemoglobin within the red cells. We present measurements using a microfluidic method we have developed to determine the pressure required to eject individual red cells from a capillary-sized channel after the cell has sickled. We find that the maximum pressure is only ∼100 Pa, much smaller than typically found in the microcirculation. This explains why experiments using animal models have not observed occlusion beginning in capillaries. The magnitude of the pressure and its dependence on intracellular concentration are both well described as consequences of sickle hemoglobin polymerization acting as a Brownian ratchet. Given the recently determined stiffness of sickle hemoglobin gels, the observed obstruction seen in sickle cell disease as mediated by adherent cells can now be rationalized, and surprisingly suggests a window of maximum vulnerability during circulation of sickle cells.
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