Table 1

Lack of effect of ARL 15896AR in the two-vessel occlusion/hypotension model of global ischemia (12 min): evaluation of rat CA1 hippocampal and striatal neurons

ExperimentalHippocampal CA1 NeuronsStriatal Neurons
VehicleARL 15896ARVehicleARL 15896AR
Pentobarbital
Anesthesia—I1-a
ARL 15896AR2.7  ± 0.913.0  ± 0
(500 ng/ml)(n  = 10)(n  = 3)
ARL 15896AR2.5  ± 0.95
(1000 ng/ml)(n  = 12)
Pentobarbital
Anesthesia—II1-b
ARL 15896AR61.1%  ± 1069.5%  ± 870  ± 251-c 92  ± 32
(12 mg/kg, b.i.d./(n  = 6)(n  = 7)(n  = 6)(n  = 7)
7 days, s.c.)
Nitrous oxide/
halothane anesthesia1-b
ARL 15896AR53.7%  ± 1845%  ± 1184  ± 231-c 52  ± 15
(24 mg/kg, b.i.d./(n  = 5)(n = 9)(n  = 5)(n  = 9)
7 days, p.o.)
  • Values are the combined means ± S.E. of all levels of sections including left and right sides of the brain.

  • 1-a In the pentobarbital anesthesia–I study hippocampal CA1 neuronal damage is quantified using a gross scoring technique rating bilaterally 6 sections taken along the mid-septotemporal hippocampus: 3 = 67–100%, 2 = 34–66%, 1 = <33% and 0 = no damage.

  • 1-b In the pentobarbital anesthesia–II study and with the nitrous oxide/halothane anesthesia study, the hippocampus is examined at six levels along the septotemporal axis. Damage at each level is expressed as a percentage of the total CA1 setter (see “Methods”).

  • 1-c Striatal damage is quantified by examination of two 630-μm diameter microscopic fields in the dorsolateral caudate at the coronal level of septal nuclei (+0.2 mm from Bregma). Values represent total number of acidophilic neurons in the two fields.