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Red Blood Cell Deformability, Vasoactive Mediators, and Adhesion, McMahon, 2019

Discussion in 'Other health news and research' started by SNT Gatchaman, Nov 8, 2021.

  1. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    Red Blood Cell Deformability, Vasoactive Mediators, and Adhesion
    Timothy J. McMahon
    Open Access

    Healthy red blood cells (RBCs) deform readily in response to shear stress in the circulation, facilitating their efficient passage through capillaries. RBCs also export vasoactive mediators in response to deformation and other physiological and pathological stimuli.

    Deoxygenation of RBC hemoglobin leads to the export of vasodilator and antiadhesive S-nitrosothiols (SNOs) and adenosine triphosphate (ATP) in parallel with oxygen transport in the respiratory cycle. Together, these mediated responses to shear stress and oxygen offloading promote the efficient flow of blood cells and in turn optimize oxygen delivery.

    In diseases including sickle cell anemia and conditions including conventional blood banking, these adaptive functions may be compromised as a result, for example, of limited RBC deformability, impaired mediator formation, or dysfunctional mediator export. Ongoing work, including single cell approaches, is examining relevant mechanisms and remedies in health and disease.
     
    alktipping, sb4, Snow Leopard and 6 others like this.
  2. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

    Messages:
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    Location:
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    See also
    The Deformability of Red Blood Cells in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - Thesis: Brendan Robert Schmidt 2019
    and
    Review: Squeezing for Life – Properties of Red Blood Cell Deformability, 2018, Huisjes et al
     
  3. alex3619

    alex3619 Senior Member (Voting Rights)

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    I first encountered these ideas in connection with CFS (the favoured term in the time this was going on) in the late 90s. Stanford (Open Medicine Foundation?) did some preliminary experiments in recent years and could not find the problem if I am interpreting what I recall correctly. However its possible it exists and needs very fresh blood, especially for controls. Its also possible we are doing the wrong tests. This hypothesis with regards to ME is not dead in my opinion, but its going to take groundbreaking research to demonstrate it.

    Its a similar story for vasoactive regulators. I first ran into that hypothesis at around the same time.

    If I recall things correctly, these ideas were first championed for CFS (not the more modern views of ME) in New Zealand and Australia respectively.
     

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