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本文研究大脑组织５－ＨＴ及其代谢产物变化以及５－ＨＴ＿２受体拮抗剂赛庚啶对脑缺血损伤的防治作用。实验共分三部分，结果是：（１）在沙土鼠急性前脑缺血模型证明，缺血１０ｍｉｎ，３０ｍｉｎ，及缺血３０ｍｉｎ再灌２ｈ，可见脑组织５－ＨＴ减少，说明脑缺血时脑组织释放５－ＨＴ增加而摄取减少，５－ＨＴ代谢产物５ＨＩＡＡ缺血后也见减少，但再灌后明显增加。（２）５－ＨＬ＿２受体拮抗剂赛庚啶可减轻沙土鼠缺血５ｍｉｎ再灌７天后海马ＣＡ＿１区神经元迟发性损伤，给赛庚啶组ＣＡ＿１区神经元数为１６８．７９±６２．５／ｍｍ，而生理盐水对照组为８４．７２±８７．３１／ｍｍ。（３）赛庚啶对沙土鼠单侧脑缺血能减少脑组织水及钠含量改善脑水肿及减少脑组织Ｃａ￣（２＋）含量。从５－ＨＴ＿２受体拮抗剂的作用说明，５－ＨＴ可通过５－ＨＴ＿２介导加重脑缺血时神经元损伤，加重脑水肿和脑组织Ｃａ＿（２＋）聚积，５－ＨＴ＿２受体拮抗剂可减轻缺血性脑损伤。
This article studies the changes of brain tissue 5-HT and its metabolites and the prevention and treatment of 5-HT 2 receptor antagonist cyproheptadine on cerebral ischemic injury. The experiment is divided into three parts, the results are: (1) In the forebrain ischemic model of gerbils, 10min and 30min ischemia and 30min ischemia reperfusion 2h, we can see the brain tissue 5-HT decreased, indicating cerebral ischemia 5-HT increased release of brain tissue uptake decreased, 5-HT metabolites 5HIAA also decreased after ischemia, but significantly increased after reperfusion. (2) The 5-HL 2 receptor antagonist cyproheptadine can alleviate the delayed injury of neurons in hippocampal CA1 region 5 min after reperfusion for 5 min in gerbils, giving the number of neurons in CA 1 area of cyproheptadine group being 168.79 ± 62 .5 / mm, while the saline control group was 84.72 ± 87.31 / mm. (3) Cyproheptadine could decrease cerebral water and sodium content, improve brain edema and decrease Ca 2+ content in brain tissue in unilateral cerebral ischemia rats. The role of 5-HT 2 receptor antagonist shows that 5-HT can increase neuronal damage induced by cerebral ischemia by 5-HT 2, increase brain edema and accumulation of Ca 2+ in brain tissue, and increase the number of 5-HT 2 receptor antagonists Can reduce ischemic brain damage.