Hypothermia blunts acetylcholine increase in CSF of traumatically brain injured rats

Activation of muscarinic acetylcholine (ACh) receptors contributes to the pathophysiological consequences of moderate experimental traumatic brain injury (TBI). Hypothermia (30 degrees C) provides protection in experimental TBI. We measured ACh levels in CSF and plasma 5 min after moderate fluid per...

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Bibliographic Details
Published in:Molecular and chemical neuropathology 1993-04, Vol.18 (3), p.247-256
Main Authors: LYETH, B. G, JIANG, J. Y, ROBINSON, S. E, HONGZHI GUO, JENKINS, L. W
Format: Article
Language:English
Subjects:
Acetylcholine - blood
Acetylcholine - cerebrospinal fluid
Animals
Biological and medical sciences
Body Temperature - physiology
Brain - physiology
Brain Injuries - cerebrospinal fluid
Choline - blood
Choline - cerebrospinal fluid
Hypothermia, Induced
Medical sciences
Nervous system involvement in other diseases. Miscellaneous
Neurology
Rats
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Summary:Activation of muscarinic acetylcholine (ACh) receptors contributes to the pathophysiological consequences of moderate experimental traumatic brain injury (TBI). Hypothermia (30 degrees C) provides protection in experimental TBI. We measured ACh levels in CSF and plasma 5 min after moderate fluid percussion TBI under normothermic or hypothermic conditions, because ACh in the CSF has been correlated with the severity of behavioral deficits after TBI. Three groups were examined: TBI with hypothermic brain (30 degrees C), TBI with normothermic brain (37 degrees C), or sham TBI with normothermic brain (37 degrees C). ACh concentrations in CSF were significantly higher in 37 degrees C TBI rats, but not in 30 degrees C TBI rats compared to shams. ACh concentrations in plasma did not differ between groups. These results suggest that a contributing factor to the neuroprotective effects of moderate hypothermia in TBI may be related to the reduction of excessive ACh levels in the central nervous system following injury.
ISSN:1044-7393
2168-8729
DOI:10.1007/BF03160117