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Muscle metabolism with blood flow restriction in chronic fatigue syndrome.
Department of Exercise Science, University of Georgia, Athens, GA 30602, USA. kmccully@...
The purpose of this study was to determine whether chronic fatigue syndrome (CFS) is associated with reduced blood flow and muscle oxidative metabolism. Patients with CFS according to Centers for Disease Control criteria (n = 19) were compared with normal sedentary subjects (n = 11). Muscle blood flow was measured in the femoral artery with Doppler ultrasound after exercise. Muscle metabolism was measured in the medial gastrocnemius muscle with (31)P-magnetic resonance spectroscopy. Muscle oxygen saturation and blood volume were measured using near-infrared spectroscopy. CFS and controls were not different in hyperemic blood flow or phosphocreatine recovery rate. Cuff pressures of 50, 60, 70, 80, and 90 mmHg were used to partially restrict blood flow during recovery. All pressures reduced blood flow and oxidative metabolism, with 90 mmHg reducing blood flow by 46% and oxidative metabolism by 30.7% in CFS patients. Hyperemic blood flow during partial cuff occlusion was significantly reduced in CFS patients (P < 0.01), and recovery of oxygen saturation was slower (P < 0.05). No differences were seen in the amount of reduction in metabolism with partially reduced blood flow. In conclusion, CFS patients showed evidence of reduced hyperemic flow and reduced oxygen delivery but no evidence that this impaired muscle metabolism. Thus CFS patients might have altered control of blood flow, but this is unlikely to influence muscle metabolism. Furthermore, abnormalities in muscle metabolism do not appear to be responsible for the CFS symptoms.
PMID: 14578362 [PubMed - indexed for MEDLINE]
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Then I pulled up one of my favorites from DR Abou Donia's animal studies out of Duke University. This one correlates with the article mentioned in my previous posting about Boston study re sarin and dose responses. WE are making headway with the research but we have to make the research translate to better clinical care for the gulf war veterans! WE have waited long enough after 16 years.
From the article below: The early neuropathological changes observed after a single dose of 1 x LD(50) sarin could lead to a profound long-term neurodegenerative changes in many regions of the brain, and resulting behavioral abnormalities
Now if the sarin does this in the brain then the factors I mentioned above re oxygenation, RBC, hypercoagulation will certainly not help in maintaining normal blood flow in the brain and the oxygen delivery in the brain. This would seem to be a big factor! In effecting high level thought processes and in behavior. This is physiological.
Now veterans let us reflect back how many of you noticed behavioral changes in your peers while we were in Saudi/Iraq? Can you write down what you remember observing....and include when and where....and how the behavior was weird or whatever? How long had you known your peer before the war? Had you seen that type of behavior before? Did the incident occur after alarms? Do you remember any odors at the time? Did you remember fine mist? Anything else?
This is like when we have a patient that experience a concussion from a car accident etc and we see them in the ER
and the patient is not acting like himself....and the family or friend mentions it re he is not acting like himself....that is one reason we keep patients and monitor them or if they are sent home there are explicit instructions to family and friends to monitor them for awakeness, responsiveness, alertness,
The patient may have a bleed....but definitely the concussion alters there blood flow and the edema from the trauma will affect there oxygenation in the area affected....WEll this is as close as I can get to explaining so you might understand...I hope it helps.....
Now I really want the veterans to think and share what behavioral type changes you saw and when and where.
send your thoughts to DSNurse@...
Acute exposure to sarin increases blood brain barrier permeability and induces neuropathological changes in the rat brain: dose-response relationships.
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
We hypothesize that a single exposure to an LD(50) dose of sarin induces widespread early neuropathological changes in the adult brain. In this study, we evaluated the early changes in the adult brain after a single exposure to different doses of sarin. Adult male rats were exposed to sarin by a single intramuscular injection at doses of 1, 0.5, 0.1 and 0.01 x LD(50). Twenty-four hours after the treatment, both sarin-treated and vehicle-treated (controls) animals were analyzed for: (i) plasma butyrylcholinesterase (BChE) activity; (ii) brain acetylcholinesterase (AChE) activity, (iii) m2 muscarinic acetylcholine receptor (m2 mAChR) ligand binding; (iv) blood brain barrier (BBB) permeability using [H(3)]hexamethonium iodide uptake assay and immunostaining for endothelial barrier antigen (EBA); and (v) histopathological changes in the brain using H&E staining, and microtubule-associated protein (MAP-2) and glial fibrillary acidic protein immunostaining. In animals treated with 1 x LD(50) sarin, the significant changes include a decreased plasma BChE, a decreased AChE in the cerebrum, brainstem, midbrain and the cerebellum, a decreased m2 mAChR ligand binding in the cerebrum, an increased BBB permeability in the cerebrum, brainstem, midbrain and the cerebellum associated with a decreased EBA expression, a diffuse neuronal cell death and a decreased MAP-2 expression in the cerebral cortex and the hippocampus, and degeneration of Purkinje neurons in the cerebellum. Animals treated with 0.5 x LD(50) sarin however exhibited only a few alterations, which include decreased plasma BChE, an increased BBB permeability in the midbrain and the brain stem but without a decrease in EBA expression, and degeneration of Purkinje neurons in the cerebellum. In contrast, animals treated with 0.1 and 0.01 x LD(50) did not exhibit any of the above changes. However, m2 mAChR ligand binding in the brainstem was increased after exposure to all doses of the sarin.Collectively, the above results indicate that, the early brain damage after acute exposure to sarin is clearly dose-dependent, and that exposure to 1 x LD(50) sarin induces detrimental changes in many regions of the adult rat brain as early as 24 hours after the exposure. The early neuropathological changes observed after a single dose of 1 x LD(50) sarin could lead to a profound long-term neurodegenerative changes in many regions of the brain, and resulting behavioral abnormalities.
PMID: 12150792 [PubMed - indexed for MEDLINE]
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