Relationship between putrescine content and density of ischemic cell damage in the brain of mongolian gerbils: effect of nimodipine and barbiturate.

Twenty mongolian gerbils were anesthetized (1.5% halothane) and severe forebrain ischemia was produced in 15 animals by occluding both common carotid arteries. After 5 min ischemia brains were recirculated spontaneously. Immediately after ischemia nimodipine (1.5 mg/kg) or pentobarbital (50 mg/kg) was injected intraperitoneally into five animals. Four days later animals were reanesthetized (1.5% halothane); the brains were frozen with liquid nitrogen and cut in a cryostat. Ten-micrometer-thick coronal cryostat sections were stained with cresyl violet to assess the extent of ischemic cell damage in the lateral striatum, the CA1-layer of the hippocampus, and the thalamus. In addition, tissue samples (about 4 mg each) were taken from the lateral striatum, CA1 layer of the hippocampus and the thalamus. Putrescine levels were measured in these samples using reversed-phase high performance liquid chromatography and fluorescence detection. Reversible cerebral ischemia produced a significant increase in putrescine in the lateral striatum (from 11.15 +/- 0.79 to 44.83 +/- 11.76 nmol/g, P less than or equal to 0.05), the CA1 subfield of the hippocampus (from 11.27 +/- 0.64 to 41.80 +/- 3.62 nmol/g, P less than or equal to 0.05) and less so in the thalamus (from 11.28 +/- 0.70 to 16.50 +/- 1.71 nmol/g).(ABSTRACT TRUNCATED AT 250 WORDS)