http://www.karger.com/Article/FullText/15941
Abstract
Within the past few years, a growing body of evidence has
accumulated indicating that exogenously administered neurotrophic growth
factors may limit the extent of acute ischemic neural injury and
enhance functional neurorecovery following stroke. One of the most
widely studied growth factor in this regard is basic fibroblast growth
factor (bFGF). In preclinical studies, bFGF administered intravenously
within hours after the onset of ischemia reduces infarct size,
presumably due to direct protection of cells at the borders (penumbra)
of cerebral infarction. On the other hand, if bFGF is administered
intracisternally starting at one day after ischemia, infarct size is not
reduced, but recovery of sensorimotor function of the impaired limbs is
increased, presumably due to enhancement of new neuronal sprouting and
synapse formation in the intact uninjured brain. Clinical trials of the
intravenous administration of bFGF as a cytoprotective agent in acute
stroke are in progress. Trials of the delayed administration of bFGF as a
recovery-promoting agent in subacute stroke are anticipated.
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