Propofol prevents delayed neuronal death following transient forebrain ischemia in gerbils

Abstract

Purpose: This study was conducted to ascertain whether propofol may protect against delayed neuronal death in the hippocampal CAI subfield in gerbils. Methods: Thirty-five gerbils were randomly assigned to five groups: Group I, the control group, a sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg · kg-1 propofol; Group IV, ischemia/reperfusion treated with 100 mg · kg-1 propofol; Group V, ischemia/reperfusion treated with 150 mg · kg-1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N2O/O2/halothane anesthesia after administration of propofol or PSS. Five days later, histopathological changes in the hippocampal CAI subfield were examined using a light microscope and degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cells/total number of pyramidal cells per 1 mm of hippocampal CAI subfield) x 100. Results: In group II, the pyramidal cells were atrophic and pycnotic; vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; group I: 5.9 ± 1.9%, group II: 94.6 ± 2.5% (P < 0.01) group III: 10.7 ± 1.7%, group IV: 9.7 ± 1.8%, group V: 9.2 ± 1.9%. Conclusion: This study suggests that propofol may prevent delayed neuronal death in the hippocampal CAI subfield after cerebral ischemia/reperfusion in gerbils.