Treatment with basic fibroblastic growth factor following focal cerebral ischemia does not prevent neuronal injury.
This experiment determined if postischemic administration of basic fibroblast growth factor (bFGF) would result in neovascularization to minimize neuronal injury following a focal cerebral ischemia insult. Fifty-eight Sprague-Dawley rats underwent middle cerebral artery (MCA) occlusion and were divided into three groups receiving either vehicle, serum, or 50 ng bFGF biweekly through an indwelling ventricular cannula. At variable time intervals, the animals underwent carbon black perfusion of capillary beds and histological staining for assessment of neuronal injury. Following MCA occlusion, there was a significant decrease in capillary bed density in peri-infarction cortex which normalized by two weeks. The number of alive neurons in the peri-infarction cortex was also significantly decreased compared to contralateral control cortex. The chronic administration of bFGF commencing two days after MCA occlusion did not result in either a significant increase in capillary bed density or the number of alive neurons in the peri-infarction cortex.
Tenjin
H
H
Department of Neurosurgery, Mayo Clinic, Rochester, MN 55905, USA.
Anderson
R E
RE
Meyer
F B
FB
D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy* / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D002536:Cerebral Arteries / Q000502:physiology; D016222:Fibroblast Growth Factor 2 / Q000008:administration & dosage / Q000627:therapeutic use*; D007276:Injections, Intraventricular; D008297:Male; D009389:Neovascularization, Pathologic / Q000473:pathology; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D016222:Fibroblast Growth Factor 2