INTRAVENOUS BASIC FIBROBLAST-GROWTH-FACTOR DOES NOT AMELIORATE BRAIN INJURY RESULTING FROM TRANSIENT FOCAL ISCHEMIA IN CATS

This study sought to test the hypothesis that intravenous basic fibrob last growth factor (bFGF) inhibits the development of brain injury dur ing transient focal ischemia. Halothane-anesthetized cats (n = 39) und erwent left middle cerebral artery occlusion for 60 minutes. After the onset of reperfusion, wounds were closed and the cats were allowed to emerge from anesthesia. Experimental cats were treated with intra ven ous bFGF at a dose of either 2 or 5 mu g/kg per hour, beginning 45 min utes after initiation of ischemia and continuing until 24 hours of rep erfusion, when neurologic function and infarction volume were evaluate d. The cats in the control group received diluent. Three of thirteen c ats treated with bFGF 2 mu g/kg/hour and six of sixteen cats treated w ith bFGF 5 mu g/kg/hour died during the 24 hour reperfusion period. Th ere was no difference in injury volume or neurologic evaluation score in the control group (n = 10; hemisphere injury, 1301 +/- 306 mm(3,) m ean+/-SE; score 53 +/- 3), and cats treated with either 2 mu g/kg/hour (n = 10; hemisphere injury, 1170 +/- 292 mm(3); score 50 +/- 3) or 5 mu g/kg/hour bFGF (n = 10, hemisphere injury, 1343 +/- 374 mm(3); scor e 50 +/- 2). The data collected do not support the hypothesis that int ravenous bFGF is neuroprotective in a cat model of transient focal isc hemia.