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

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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 ,此时若应用M受体拮抗剂时应加大剂量 Objective To investigate the changes of M receptor in forebrain during cardiac arrest (CA) and before and after cardiopulmonary resuscitation (CPR). Methods Fifty five Wistar rats were randomly divided into normal control group (n = 8), operation control group (n = 7), CA1 group (n = 8) (N = 8): Asphyxia 20min and CA3 group (n = 8): Asphyxiation 30min and CPR preconditioning group (n = 8): Asphyxia 10min and post CPR group (n = 9) Mechanical ventilation was continued for 30 min after the circulation was recovered. At the end of the experiment, the brain was decapitated and the maximal binding capacity (Bmax) and equilibrium dissociation constant (KD) of M receptor in the forebrain were determined by radioligand binding assay. Results Asphyxial rats CA required about 5min. Compared with the normal control group, Bmax in CA3 group was significantly increased (P <0.01) and KD value was not significantly changed (P> 0.05); Bmax and KD in the control group, CA1 group and CA2 group No significant difference (P> 0.05). There was no significant difference in Bmax between the CPR group and the pre-CPR group (P> 0.05), but the KD value was significantly increased (P <0.01). Conclusion Asphyxiation caused 25 min after CA, while the density of M receptor in forebrain increased while the affinity remained unchanged. At this point if the application of M receptor antagonist may be beneficial to CPR and brain function protection; CPR, M receptor antagonist frontal brain decreased affinity at this time if the application of M receptor antagonist should increase the dose
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