Stroke, Vol 22, 84-89, Copyright © 1991 by American Heart Association
S Yoshida, T Kirino, A Tamura, N Basugi and K Sano
It has been proposed that lithium ion desensitizes neuronal receptors that
function via the inositol phospholipid signaling mechanism. We examined the
effects of lithium chloride on the morphologic outcome after 5 minutes of
cerebral ischemia induced in gerbils by occluding both common carotid
arteries under brief halothane anesthesia. In three treated groups of 10
gerbils each, 5 meq/kg i.p. lithium chloride was given 2 days, 1 day, and 2
hours before ischemia; 2 hours before ischemia; or immediately after the
end of ischemia. Corresponding control groups of nine or 10 gerbils each
received equivalent volumes of saline injected at comparable times. All
gerbils were perfusion- fixed 1 week later, and neuronal density of the
hippocampal CA1 pyramidal cells was determined. Lithium induced very mild
intraischemic systemic hypothermia, but postischemic hyperthermia developed
in both treated and control groups. Neuronal densities were equal in
corresponding groups. The results indicate that our regimen of lithium
administration provides no benefit in survival of hippocampal neurons, and
intraischemic hypothermia of less than 0.8 degrees C is not protective.
Other strategies to inactivate the signal transduction system that is
specific for excitatory neurotransmission should be evaluated.
ARTICLES
Lithium ion does not protect brain against transient ischemia in gerbils
Department of Neurosurgery, Kanto Rosai Hospital, Kawasaki, Japan.
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  M. Ren, V. V. Senatorov, R.-W. Chen, and D.-M. Chuang Postinsult treatment with lithium reduces brain damage and facilitates neurological recovery in a rat ischemia/reperfusion model PNAS, May 13, 2003; 100(10): 6210 - 6215. [Abstract] [Full Text] [PDF]
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