This study tested the hypothesis that
lidoflazine, a
calcium entry blocking
drug, will improve post-ischemic neurologic outcome when administered after a period of complete
cerebral ischemia, and that the improvement in outcome is related to an increase in post-ischemic cerebral blood flow (CBF). Complete
cerebral ischemia was produced in 31 dogs by temporary
ligation of the aorta and venae cavae. In six dogs, 10 min of complete
cerebral ischemia was followed by an infusion of
lidoflazine 1.0 mg X kg-1 iv over 10 min. CBF and cerebral metabolic rate for
oxygen (CMRO2) were measured pre-
ischemia, and for 90 min post-
ischemia. The results from these six dogs were compared with results previously obtained from eight untreated dogs under similar, but not identical, conditions. The CBF measured post-
ischemia in the dogs administered
lidoflazine did not differ from the CBF measured post-
ischemia in the untreated dogs. Both groups showed an initial
hyperemia post-
ischemia, followed by significant decreases in CBF from control values by 35 min post-
ischemia. The post-ischemic CMRO2 also did not differ between
lidoflazine treated and untreated groups. In 25 dogs, 11 min of complete
cerebral ischemia was followed by an iv infusion of either
lidoflazine 1.0 mg X kg-1 or saline placebo. The same iv infusions were repeated at 8 and 16 h post-
ischemia. Seven dogs were excluded from data analysis for failure to meet pre-established protocol criteria. Neurologic injury was evaluated in the remaining dogs at 48 h post-
ischemia by an observer blinded to the treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)