Publication: Amplification of inhibitory mechanisms in cerebral ischemia: an alternative approach to neuronal protection
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Date
1997
Authors
Shuaib, A. ; Kanthan, R.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The central nervous systern consumes 20%
of the cardiac output for normal function. The neurons
are very sensitive to the effects of ischemia. Cessation of
cerebral blood flow results in severe damage to neurons
and other brain structures. This is secondary to a
combination of energy loss, excessive excitation
promoting intracellular calcium (ca2+) buildup, relative
lack of inhibitory responses, generation of oxygen free
radicals (especially during the reperfusion period) and
severa1 other destructive cascades. Medications that
antagonize the effects of glutamate at post-synaptic
receptors are either ineffective or have serious sideeffects.
ca2+ entry blockers have shown disappointing
results in clinical trials in patients with acute cerebral
infarction. Data with protective effects of oxygen free
radical scavengers in the post-ischemic period have
shown conflicting results.
There is recent interest with the use of agents that
increase cerebral inhibitory responses after an ischemic
insult. Such agents are effective when used before,
during or up to 4 hours after the ischemic insult. Many
such rnedications have few side-effects and are in
clinical use for other indications. This review will
surnmarize inhibitory rnechanisms that may be important
in cerebral ischernia, and provide experimental evidence
for their potential efficacy.
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