Altered Erythrocyte Biophysical Properties in Chronic Fatigue Syndrome, 2019, Saha, Davis, et al

Conference Abstract : RED BLOOD CELL BIOMECHANICS IN CHRONIC FATIGUE SYNDROME
Amit K. Saha et al

Summer Biomechanics, Bioengineering and Biotransport Conference
June 25 -28, Seven Springs, PA, USA
https://www.researchgate.net/public...Cell_Biomechanics_in_Chronic_Fatigue_Syndrome

Introduction
....
In the present work, we focus on the pathophysiological changes in red blood cells (RBCs) since CFS is a systemic disease rather than of a particular organ or tissue, and RBCs, comprising ~45% of blood volume, are responsible for microvascular perfusion and tissue oxygenation.

RBCs deform and travel through microvessels smaller than their diameter to facilitate the optimal transfer of gases between blood and tissue. The usual shape of a RBC is a biconcave discoid, which is changed to an ellipsoid due to shear flow.

This shape gives them a specific surface area-to-volume ratio which facilitates large reversible deformations and elastic transformation [3].

We used a high throughput microfluidic platform to assess the changes in RBC deformability between CFS patients and matching healthy controls. We also performed computational studies to have a better understanding of the cell deformation.

In order to explore the mechanisms for observed changes in cell deformability, we explored the membrane fluidity, reactive oxygen species, and surface charge, of RBCs.
 
They were presenting the same study at the conference as the one of this thread but with additional data on membrane fluidity, reactive oxygen species, and surface charge, of RBCs, and modelling.

They are also working on a follow up study with a new cohort of patients that measures more parameters
 
This looked to be significant new information
The reactive oxygen species (ROS) contents were estimated using Di(Acetoxymethyl Ester) (6-Carboxy-2',7'-Dichlorodihydrofluorescein Diacetate) (Thermofisher Scientific). This non-fluorescent molecule is converted to a fluorescent form due to the removal of acetate groups by ROS
Reactive oxygen species (ROS). Higher levels of ROS were detected in RBCs from CFS patients as compared to healthy controls (Fig. 3).
upload_2019-7-17_14-6-17.png
 
Fits well with that metabolomics dataset that showed reduce vitamin E metabolites or something? Vitamin E is important for protecting cell membranen from oxidative damage. Not to say that ME patients have a diet deficient in vitamin E, but we might have increased need for that and some other stuff I'm too tired to write about to protect our cella against whatever is going wrong.
 
Earlier in this thread it was said that capillary diameters cannot be increased so best to focus on improving RBC deformability. I am just wandering, could increased vasodialation as seen in POTS be some kind of attempt to increase capillary diameter or is this just not possible?
 
Earlier in this thread it was said that capillary diameters cannot be increased so best to focus on improving RBC deformability. I am just wandering, could increased vasodialation as seen in POTS be some kind of attempt to increase capillary diameter or is this just not possible?
Interesting question. Here's an answer I found:

Capillaries are the smallest blood vessels. They are unique in that:

  1. They don't have any muscular component like arterioles or venules do.
  2. They are lined by a single layer of endothelium (cells lining blood vessels are called endothelial cells) overlying the basement membrane.
Due to these reasons the capillaries are very permeable facilitating nutrient and gas exchange.

The capillaries don't expand as they do not have muscular or elastic components. However exposure to heat do increase the circulation. This is due to the following facts:

  1. Exposure to heat dilates the pre-capillary arterioles - this would inevitably cause improved capillary circulation in capillaries that are already open.
  2. Increase in pre-capillary flow opens up collapsed capillaries. In the human body roughly only one-fourth of the capillaries are open during rest1. As the pre-capillary arterioles dilate, the collapsed capillaries open up thus further improving circulation.
To improve capillary perfusion:

  • Temporary improvement can be achieved by activity (exercise), exposure to warmth, emotions (flushing is due to vasodilation), even exposure to cold causes vasodilation after the initial vasoconstriction
  • Permanent improvement of capillary circulation can be achieved by increasing capillary density. Capillary density refers to the number of capillaries present in 1 cm2 area. Capillary density can be increased by consistent anaerobic (isometric and to some extent isotonic) exercise.
References:
1: Boron and Boupaep text book of medical physiology, 2nd Edition, p.467

https://biology.stackexchange.com/questions/28258/blood-circulation-how-to-expand-blood-capillaries
 
I am just wandering, could increased vasodialation as seen in POTS be some kind of attempt to increase capillary diameter or is this just not possible?

from the related thread:

So red blood cells release ATP when they sense hypoxic tissues (this occurs during exercise when muscles require more oxygen) but also apparently when they are mechanically deformed (squeezed). That released ATP activates the synthesis of vasodilators including nitric oxide which then increase the size of blood vessels so more blood can flow.
 
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