nor－BNI拮抗不同剂量强啡肽A_（1－13）及A_（2－17）鞘内注射致瘫

COMPARISON OF THE ANTAGONISM OF NOR-BNI TO THE PARALYSIS CAUSED BY DIFFERENT DOSES OF INTRATHECAL DYN A(1-13)AND DYN A(2-17)

利用ＳＤ大鼠，观察了预先鞘内注射阿片肽Ｋ受体拮抗剂ｎｏｒ－ＢＮＩ拮抗不同剂量ＤｙｎＡ＿（１－１３）及ＤｙｎＡ＿（２－１７）蛛网膜下腔注射致瘫的结果。结果表明：ｎｏｒ－ＢＮＩ能对抗低剂量，而不能对抗高剂量ＤｙｎＡ＿（１－１３）所致瘫痪；ＤｙｎＡ＿（２－１７）不作用于阿片受体，其鞘内注射仍能引起双后肢瘫痪，ｎｏｒ－ＢＮＩ对其无拮抗作用。结果提示：强啡肽Ａ在脊髓继发性损伤中的作用除经由阿片肽Ｋ受体介导外，尚存在非阿片样介导途径，强啡肽Ａ的致瘫机理是阿片样和非阿片样联合作用的结果。

It was observed that pretreatment with kappa opiate receptor antagonist nor-BNIantagonized the paralysis caused by intrathecal dyn A(1-13)or dyn A(2-17).The re-sults showed that nor-BNI can antagonize the paralysis caused by low doses of dyn A(1-13).Although intrathecal dyn A(2-17) dose not act on the opiate receptor,it canalso cause paralysis,which can not be antagonized by nor-BNI. The experiment confir-med that dynorphine contributes to certain pathophysiological changes after traumaticspinal cord injury through both opiate-receptor(k-receptor mediated and nonopioid me-chanisms.