BACKGROUND AND PURPOSE: The aim of this study was to ascertain whether basic fibroblast growth factors (bFGF) caused reduction in size of cerebral infarcts in Sprague-Dawley rats with experimental ischemia. METHODS: In the first experiment we induced permanent occlusion of the left middle cerebral artery (MCA). Within 5 minutes after MCA occlusion, we infused bFGF (100 ng in 0.1 mL of saline) in the bFGF-treated group (n = 14) and 0.1 mL of saline alone in the control group (n = 7) into the common carotid artery ipsilateral to MCA occlusion. We harvested the brains 24 hours after MCA occlusion and determined infarct size planimetrically as a percentage of hemisphere size. In the second experiment cerebral blood flow (CBF) was continuously measured for 120 minutes after MCA occlusion in the bFGF-treated group (n = 9) and in the control group (n = 8) with the use of laser-Doppler flowmetry. RESULTS: Infarct size in the bFGF-treated group decreased significantly in comparison with that in the control group (repeated-measures ANOVA, P < .0001). CBF in the transitional areas between the MCA and the anterior cerebral artery significantly increased in the bFGF-treated group in comparison with that in the control group (repeated-measures ANOVA, P < .005). An approximate 58% decrease in infarct size and a 40% increase in regional CBF were seen on bFGF treatment. CONCLUSIONS: The present study suggested that intracarotid administration of bFGF (100 ng) can reduce infarct size after MCA occlusion. It was speculated that the increased CBF in the penumbral areas of MCA may contribute to contraction of infarct size.
BACKGROUND AND PURPOSE: The aim of this study was to ascertain whether basic fibroblast growth factors (bFGF) caused reduction in size of cerebral infarcts in Sprague-Dawley rats with experimental ischemia. METHODS: In the first experiment we induced permanent occlusion of the left middle cerebral artery (MCA). Within 5 minutes after MCA occlusion, we infused bFGF (100 ng in 0.1 mL of saline) in the bFGF-treated group (n = 14) and 0.1 mL of saline alone in the control group (n = 7) into the common carotid artery ipsilateral to MCA occlusion. We harvested the brains 24 hours after MCA occlusion and determined infarct size planimetrically as a percentage of hemisphere size. In the second experiment cerebral blood flow (CBF) was continuously measured for 120 minutes after MCA occlusion in the bFGF-treated group (n = 9) and in the control group (n = 8) with the use of laser-Doppler flowmetry. RESULTS:Infarct size in the bFGF-treated group decreased significantly in comparison with that in the control group (repeated-measures ANOVA, P < .0001). CBF in the transitional areas between the MCA and the anterior cerebral artery significantly increased in the bFGF-treated group in comparison with that in the control group (repeated-measures ANOVA, P < .005). An approximate 58% decrease in infarct size and a 40% increase in regional CBF were seen on bFGF treatment. CONCLUSIONS: The present study suggested that intracarotid administration of bFGF (100 ng) can reduce infarct size after MCA occlusion. It was speculated that the increased CBF in the penumbral areas of MCA may contribute to contraction of infarct size.