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Chronic Fatigue Syndrome/ME Fibromyalgia
 

Evidence that heightened pain perception in CFS is linked to oxidative stress

  (6 votes)
ProHealth.com • November 10, 2012

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Article:
Modulation of the Axon-Reflex Response to Local Heat by Reactive Oxygen Species (ROS) in subjects with Chronic Fatigue Syndrome
- Source: Journal of Applied Physiology, Nov 8, 2012

By Marvin S Medow, PhD, et al.

[Note: Dr. Medow's research specialties include CFS, orthostatic dysfunction, nutrition, and cellular structure & function. Reactive oxygen species (ROS) are reactive molecules/free radicals – unstable molecules lacking an oxygen atom that are a byproduct of mitochondrial energy production. If not recycled by antioxidants, such as glutathione (which are able to donate a stabilizing oxgen atom to them without themselves becoming unstable), ROS steal oxygen atoms from other molecules in the cell, which in turn are unstabilized, and so on, creating a cell damaging chain reaction. This state is called “oxidative stress.”]

Abstract:
Local cutaneous heating causes vasodilation as an initial first peak, a nadir, and increase to plateau. Reactive oxygen species (ROS) modulate the heat plateau in healthy controls. The initial peak, due to C-fibre nociceptor-mediated axon reflexes, is blunted with local anesthetics, and may serve as a surrogate for the cutaneous response to peripheral heat.

Chronic Fatigue Syndrome (CFS) subjects report increased perception of pain.

To determine the role of ROS in this neurally-mediated response, we evaluated changes in cutaneous blood flow from local heat in 9 CFS subjects (16-22 years) compared to 8 healthy controls (18-26 years).

We heated skin to 42°C and measured local blood flow as a percentage of maximum cutaneous vascular conductance (%CVC(max)).

While CFS subjects had significantly lower baseline flow (8.75+/-0.56 vs. 12.27+/-1.07 (%CVC(max) , CFS vs. control)), there were no differences between groups to local heat.

We then re-measured this with apocynin to inhibit NADPH oxidase, allopurinol to inhibit xanthine oxidase, tempol to inhibit superoxide, and ebselen to reduce H(2)O(2).

Apocynin significantly increased baseline blood flow (before heat, 14.91+/-2.21 vs. 8.75+/-1.66) and the first heat peak (69.33+/-3.36 vs. 59.75+/-2.75).

Allopurinol and ebselen only enhanced the first heat peaks (71.55+/-2.48 vs. 61.72+/-2.01 and 76.55+/-5.21 vs. 58.56+/-3.66, respectively).

Tempol had no effect on local heating.

None of these agents changed the response to local heat in control subjects.

Thus the response to heat may be altered by local levels of ROS, particularly H(2)O(2) [hydrogen peroxide] in CFS subjects, and may be related to their hyperesthesia/ hyperalgesia [abnormally increased sensitivity/pain perception].

Source: Journal of Applied Physiology, Nov 8, 2012. PMID:23139367, by Medow MS, Aggarwal A, Baugham IL, Messer ZR, Stewart JM. New York Medical College, Valhalla, New York, USA. [Email: marvin_medow@nymc.edu]




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