Anisodamine protects against neuronal death following cerebral ischemia in gerbils

Objective To study the effect of anisodamine on neuronal death and hydroxyl radical (OH·) production during forebrain ischemia-reperfusion in gerbils. Methods The tested gerbils were divided into 3 groups, including sham-operated, control and anisodamine groups. In each group, there were 8 animals for biochemical examination and 6 animals for histologic study. Forebrain ischemia was induced by occlusion the bilateral common carotid arteries for 10 min in gerbils. 2,3- and 2,5-DHBA outputs were determined by high performance hiquid chromatography coupled with electrochemical detection. Behavioral change was tested by open field test and neuronal death was assessed by histological examination.Results The exploratory activities of gerbils in the control group were significantly higher than those in the anisodamine group on all test days. The amount of viable-looking neurons in the medial, middle and lateral CA1 sectors in anisodamine group were 41%±12%, 50%±21% and 67%±15% of the sham-operated gerbils, respectively, being significantly higher than those in the control group (3%±2%, 4%±3% and 7%±4% of sham, P<0.01). The 2,3-DHBA outputs in the control group increased by 5 fold of the sham-operated gerbils after reperfusion for 60 min, but the 2,3-DHBA outputs in the anisodamine group were only 2.4 fold of sham-operated gerbils, being significantly lower than that in the control group (P<0.01). The 2,5-DHBA outputs in the control group were significantly higher than those in the sham-operated group (P<0.05). Conclusion Anisodamine has inhibitory effects on neuronal death and OH·production during cerebral ischemia-reperfusion in gerbils.