心跳骤停期间及心肺复苏前后前脑M受体变化的实验研究  

Changes of muscarinic acetylcholine receptor during the asphyxiation induced cardiac arrest and cardiopulmonary resuscitation in rat forebrain

作　　者：陈东升[1] 李利华[2] 武建军[2] 张颖丽[2] 

机构地区：[1]第一军医大学南方医院急诊部,广州510515 [2]中国人民解放军总医院急诊科

出　　处：《中华麻醉学杂志》2000年第2期102-104,共3页Chinese Journal of Anesthesiology

摘　　要：目的　探讨心跳骤停 (CA)期间及心肺复苏 (CPR)前后前脑M受体变化的规律。方法　采用窒息致大鼠CA的动物模型 ,5 5只Wistar大鼠随机分为正常对照组 (n =8)、手术对照组 (n =7)、CA1组 (n =8) :窒息 10min ,CA2组 (n =8) :窒息 2 0min及CA3组 (n =8) :窒息 30min ,以及CPR前组(n =8) :窒息 10min和CPR后组 (n =9) :窒息 10min后复苏 ,自主循环恢复后继续机械通气 30min ,实验结束时断头取脑 ,应用放射性配基受体结合分析法测定前脑M受体的最大结合容量 (Bmax)和平衡解离常数 (KD 值 )。结果　窒息致大鼠CA约需 5min。与正常对照组相比 ,CA3组的Bmax显著升高 (P<0 0 1)而KD 值无显著性变化 (P >0 0 5 ) ;手术对照组、CA1组及CA2组的Bmax及KD 值均无显著性差异 (P >0 0 5 )。与CPR前组前相比 ,CPR后组的Bmax无显著性差异 (P >0 0 5 ) ,而KD 值显著升高(P <0 0 1)。结论　窒息引起CA后 2 5min ,前脑M受体密度增高而亲和力不变。此时若应用M受体拮抗剂可能有利于CPR和脑功能保护 ;CPR后 ,前脑M受体对拮抗剂的亲和力降低 。Objective To investigate the changes of muscarinic acetylcholine receptor(MAChR) during cardiac arrest (CA) and cardiopulmonary resuscitation(CPR) Methods The animal model of CA was established by clamping endotracheal tube at the end expiration Fifty five Wistar rats were randomly divided into 6 groups: normal control group (NC,n=8), sham operated group (SO,n=7) and CA1 group(n=8): 10 min asphyxiation, CA2 group(n=8):20 min asphyxiation ,CA3 group(n=8):30 min asphyxiation, pre CPR group (n=8):10 min asphyxiation and post CPR group: 30 min ventilation after resuscitation following 10 min asphyxiation At the end of experiment the rats were decapitated to detect maximum binding capacity (Bmax) and K D value of MAChR in forebrain using radioligand receptor binding assay Results The animal model of asphyxiation induced CA could be established in 5 min As compared with those in NC group, Bmax increased significantly (P<0 01),but K D value was kept stable in CA3 group(P>0 05) ; Bmax and K D value remained unchanged markedly in the groups of SO,CA1 and CA2 (P>0 05) In comparison with those in pre CPR group,Bmax changed unsignificantly (P>0 05), but K D value significantly increased (P<0 01) in post CPR group Conclusions MAChR density in forebrain increases ,but the affinity dose not change 25 min following asphyxiation induced CA ,indicating that administration of MAChR antagonist may be beneficial for CPR After CPR,the affinity of MAChR to antagonist in forebrain decreases, suggesting that MAChR antagonist , if required, should be administered at the higher dosage

关 键 词：心脏骤停 心肺复苏术 前脑M受体 

分 类 号：R605.974[医药卫生—急诊医学] R541.780.5[医药卫生—外科学]