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Anisodamine protects against neuronal death following cerebral ischemia in gerbils
1Department of Anesthesiology, Jiangsu Provincial Key Laboratory of Anesthesiology, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China. xmcfa@public.xz.js.cn
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 liquid 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.