Postischemic Administration of Basic Fibroblast Growth Factor Improves Sensorimotor Function and Reduces Infarct Size Following Permanent Focal Cerebral Ischemia in the Rat

2002 ◽  
Vol 177 (2) ◽  
pp. 531-537 ◽  
Author(s):  
Qiu Li ◽  
Diane Stephenson
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Infarct Size ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Sensorimotor Function ◽  
Fibroblast Growth

Pretreatment with intraventricular basic fibroblast growth factor decreases infarct size following focal cerebral ischemia in rats

1994 ◽  
Vol 35 (4) ◽  
pp. 451-457 ◽  
Author(s):  
Naoki Koketsu ◽  
David J. Berlove ◽  
Michael A. Moskowitz ◽  
Neil W. Kowall ◽  
Cornelio G. Caday ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Infarct Size ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Fibroblast Growth

scholarly journals Delayed Treatment with Intravenous Basic Fibroblast Growth Factor Reduces Infarct Size following Permanent Focal Cerebral Ischemia in Rats

1995 ◽  
Vol 15 (6) ◽  
pp. 953-959 ◽  
Author(s):  
Marc Fisher ◽  
Mary-Ellen Meadows ◽  
Tuyen Do ◽  
Jens Weise ◽  
Vladimir Trubetskoy ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Brain Temperature ◽  
Infarct Volume ◽  
Fibroblast Growth ◽  
Sprague Dawley ◽  
Arterial Blood

Basic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 μg/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague–Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 ± 1.0 in vehicle-treated and 1.5 ± 1.3 in bFGF-treated rats (mean ± SD; TV = 12 vs. 11; p = 0.009). Infarct volume was 297 ± 65 mm3 in vehicle- and 143 ± 135 mm3 in bFGF-treated animals ( p = 0.002). During infusion, there was a modest decrease in mean arterial blood pressure but no changes in arterial blood gases or core or brain temperature in bFGF-treated rats. Autoradiography following intravenous administration of 111In-labeled bFGF showed that labeled bFGF crossed the damaged blood–brain barrier to enter the ischemic (but not the nonischemic) hemisphere. Whether the infarct-reducing effects of bFGF depend on intraparenchymal or intravascular mechanisms requires further study.

scholarly journals Intracisternal Basic Fibroblast Growth Factor (bFGF) Enhances Behavioral Recovery following Focal Cerebral Infarction in the Rat

1996 ◽  
Vol 16 (4) ◽  
pp. 542-547 ◽  
Author(s):  
Takakazu Kawamata ◽  
Nancy E. Alexis ◽  
W. Dalton Dietrich ◽  
Seth P. Finklestein
Keyword(s):  
Growth Factor ◽  
Infarct Size ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neurological Deficits ◽  
Fibroblast Growth ◽  
Sprague Dawley ◽  
Behavioral Recovery

Basic fibroblast growth factor (bFGF) is a potent neurotrophic agent that promotes neuronal survival and outgrowth. Previous studies have shown that bFGF, administered intraventricularly or intravenously before or within hours after ischemia, reduces infarct size and neurological deficits in models of focal cerebral ischemia in rats. In the current study, we tested the hypothesis that bFGF, administered at later time points after ischemia, might improve behavioral recovery without affecting infarct size. Mature Sprague–Dawley rats received bFGF (1 μg/injection) or vehicle by biweekly intracisternal injection for 4 weeks, starting at 1 day following permanent proximal middle cerebral artery (MCA) occlusion. Animals were examined every other day using four different behavioral tests to assess sensorimotor and reflex function. At 4 weeks after ischemia, there was no difference in infarct volume between bFGF- and vehicle-treated animals. There was, however, an enhancement in the rate and degree of behavioral recovery among bFGF-treated animals, as measured by all four tests. There were no apparent side effects of bFGF treatment, except that bFGF-treated animals tended to recover body weight more slowly than did vehicle-treated animals following stroke. The mechanisms of enhancement of behavioral recovery by bFGF require further study, but may include protection against retrograde neuronal death and/or stimulation of neuronal sprouting.

Reduction in Myocardial Infarct Size by Basic Fibroblast Growth Factor After Temporary Coronary Occlusion in a Canine Model

Circulation ◽  
1996 ◽  
Vol 94 (8) ◽  
pp. 1927-1933 ◽  
Author(s):  
Mark C.G. Horrigan ◽  
Andrew I. MacIsaac ◽  
Francesca A. Nicolini ◽  
D. Geoffrey Vince ◽  
Philmo Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Infarct Size ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Canine Model ◽  
Myocardial Infarct Size ◽  
Fibroblast Growth
Sign in / Sign up

Export Citation Format

Share Document