Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.

Forty gerbils were randomly assigned to five groups: Group I, control, sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg x kg(-1) propofol; Group IV, ischemia/reperfusion treated with 100 mg x kg(-1) propofol; Group V, ischemia/reperfusion treated with 150 mg x kg(-1) propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N2O/O2/halothane anesthesia after propofol or PSS. Five days later, the cerebrum was removed and each forebrain was cut into two including the hippocampus. Lipid peroxidation was determined using the production of malondialdehyde (MDA), and histopathological changes in the hippocampal CA1 subfield were examined.

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. Degenerative ratios of pyramidal cells were: Group I: 4.9 +/- 2.3, Group II: 94.1 +/- 4.5 (P < 0.01), Group III: 12.5 +/- 5.7, Group IV: 11.0 +/- 4.6, Group V: 9.6 +/- 4.9%. Production of MDA was: Group I: 83 +/- 22, Group II: 198 +/- 25 (P < 0.01), Group III: 153 +/- 39, Group IV: 113 +/- 34, Group V: 106 +/- 27 nmol x g(-1) wet tissue.

Propofol attenuated delayed neuronal death by preventing lipid peroxidation induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.