摘要
目的和方法 :采用蒙古沙土鼠双侧颈总动脉结扎 (BCAO)前脑缺血模型 ,研究N 甲基D 门冬氨酸 (NMDA)受体 (NR)非竞争性拮抗剂氯胺酮 (ketamine,KT)、L 型电压门控钙离于通道 (L typevoltagegatedcalciumchannel,L型VGCC)拮抗剂硝苯吡啶 (NifedipineND)及非NR拮抗剂 6 ,7 二硝基喹恶啉上卫四 (6 ,7 dinitroquinoxaline 2 ,3dioneDNQX)对沙土鼠脑缺血及缺血 /再灌海马可溶性 (S3)、突触体 (P2 )和颗粒性 (P3)部分中磷酸酪氨酸蛋白 (p tyr pr)含量变化的影响。 结果 :①缺血 15min ,三部分 (P2 ,P3,S3) p tyr pr含量均下降 ,而S3 部分 p tyr pr含量下降更明显 ;随着脑缺血再灌时间的延长 ,三部分P tyr Pr含量均逐渐升高。S3 部分恢复快 ,P2 与P3 部分相比 ,升高的速度较慢 ,但升高的幅度较大 ,且再灌后期变化不大 ;②脑缺血前腹腔注射KT或ND ,均可部分地拮抗缺血再灌引起的p tyr pr含量的升高 ,而DNQX对此无影响。 结论 :缺血 /再灌引起的p tyr pr变化与NR通道及L型VGCC有关 。
Aim and Methods: The effects of three drugs including ketamine(KT), a noncometitive antagonist of NMDA receptor (NR),nifedipine(ND), a voltage gated calcium channel (VGCC) antagonist and 6, 7dinitroquinoxaline 2, 3 dione(DNQX), a non NMDA receptor antagonist on the contents of phospho tyrosine proteins(p tyr pr) in the synaptosomal(P 2), the crude membrane (P 3), and the cytosolic(S 3)fractions of hippocampus in forebrain ischemia of mongolian gerbils were studied.Results: ①the contents of p tyr pr in all three fractions (P 2,P 3,S 3)decreased 15 min after ischemia, but the contents of p tyr pr in S 3 fraction decreased more obviously than the others did, With the increase of reperfusion time, the contents of p tyr pr in all of these fractions recovered gradually, but the p tyr pr in S 3 fraction increased more rapidly among them, in the P 2 fraction, the contents of p tyr pr increased slowly, but signi ficantly and sustained longer during reperfusion when compared with that of P 3 did. ②The increase in p tyr pr contents induced by cerebral ischemia/reperfusion was partially antagonisted by KT and ND administration prior to cerebral ischemia, under these conditions,DNQX has no effect on it. Conclusion: the increase of p tyr Pr contents induced by cerebral ischemia/reperfusion is related to NR channel and L type VGCC,but not to non NR channel.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2001年第1期5-9,共5页
Chinese Journal of Applied Physiology
基金
国家自然科学基金资助项目!(39770 177)
