Stroke, Vol 24, 558-562, Copyright © 1993 by American Heart Association
CE Gross, MM Bednar, DB Howard and MB Sporn
BACKGROUND AND PURPOSE: The aim of this study was to examine the effect of
transforming growth factor-beta 1, a cytokine shown to amelioriate cardiac
ischemia, in a rabbit model of thromboembolic stroke. METHODS: An
autologous clot embolus was introduced intracranially through the right
internal carotid artery in 21 New Zealand White rabbits, with seven in each
group receiving either vehicle control (albumin) or 10 or 50 micrograms
transforming growth factor-beta 1 administered as an intracarotid bolus
immediately before autologous clot embolization. Multiple physiological
parameters were monitored, including regional cerebral blood flow, arterial
blood gases, hematocrit, glucose, core temperature, and mean arterial
pressure. The brain was harvested 4 hours after embolization, and infarct
size was determined planimetrically as a percentage of the entire
hemisphere. RESULTS: Brain infarct size was reduced in both the
10-microgram (16.7 +/- 4.0% [mean +/- SEM], p < 0.05) and 50-microgram
(21.7 +/- 4.5%) transforming growth factor-beta 1-treated groups when
compared with the control group (31.9 +/- 6.6%). Regional cerebral blood
flow did not show any significant intergroup or intragroup variation over
time, although the 10-microgram transforming growth factor-beta 1 group
experienced a greater return of cerebral blood flow in the first 2 hours
after embolization. CONCLUSIONS: Transforming growth factor-beta 1 reduced
brain infarct size in a rabbit model of thromboembolic stroke. This effect
was not related to a direct effect on blood flow. Studies are ongoing to
determine the mechanism by which transforming growth factor- beta 1
salvages ischemic brain.
ARTICLES
Transforming growth factor-beta 1 reduces infarct size after experimental cerebral ischemia in a rabbit model
Division of Neurosurgery, Vermont Center for Vascular Research, University of Vermont, Burlington 05401.
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