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不同剂量阿托品对右美托咪定心脏窦房结及房室结抑制作用的逆转效果

Reversal effect of atropine on the function of sinus node and the atrioventricular node inhibiting action by dexmedetomidine

来源期刊: 广州医药 | 33-36 发布时间:2021-12-01 收稿时间:2025/11/13 17:21:50 阅读量:20
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关键词:
右美托咪定阿托品窦房结房室结
DexmedetomidineAtropineSinus nodeAtrioventricular node
DOI:
10.3969/j.issn.1000-8535.2018.03.009
收稿时间:
2018-01-24 
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引用总数:
0  
目的 观察两种不同剂量的阿托品对右美托咪定心脏窦房结及房室结抑制作用的逆转效果。方法 健康志愿者20名,男12名,女8名,18~30岁。受试者先后给予右美托咪啶(1.5±0.5)μg/kg负荷量,持续泵注量(0.75±0.25)μg/(kg·h)进行试验观察。试验过程中如受试者心率<(50±5)次/分,房室结前传2∶1小于150次/分的受试者随机进入0.5 mg阿托品剂量拮抗组(A1),1 mg阿托品剂量拮抗组(A1),每组10例。与泵注前(T0),静脉泵注右美托咪定后(50±5)min(T1),阿托品静脉推注后(10±5)min(T2)经食道左心房调搏测定窦房结恢复时间(SNRT),校正窦房结恢复时间(CSNRT),房室结前传2∶1点阻滞点和房室结有效不应期(AVNERP)测量。结果 组内比较:泵注右美托咪定后T1时点与基础值T0时点比较两组窦房结及房室结功能受到抑制,SNRT 均延长(P<0.05),CSNRT比较无差异(P>0.05),房室结前传2∶1阻滞点降低(P<0.05), AVNERP延长(P<0.05)。阿托品使用后T2时点的A1组的各指标及A2组的AVNERP恢复到基础水平(P>0.05),A2组的SNRT、CSNRT均较T0时点缩短(P<0.05),A2组房室结前传2∶1阻滞点均较T0时点增高(P<0.05)。组间比较:2组T0时窦房结及房室结功能各指标比较均无差异(P>0.05),T2时点A2组SNRT、AVNERP较A1缩短(P<0.01),T2时点A2组2∶1阻滞点均较A1组增高(P<0.05)。结论 0.5 mg阿托品能逆转右美托咪定心脏窦房结及房室结抑制作用,1 mg阿托品增进右美托咪定影响下的窦房结及房室结传导功能。
Objective To investigate two different doses atropine make reverse effects on the function of sinus node and the atrioventricular node inhibiting action dexmedetomidine (Dex). Methods 20 healthy volunteers were included in the clinical trials aged 18~30 years (12 male, 8 female). The volunteers were administered with Dex at loading dose 1.5±0.5 μg/kg and then at 0.75±0.25 μg/(kg·h). During the trail, the volunteers who happened the minimal heart rate less than 50±5 bpm, atrioventricular node forward 2∶1 block point less than 150 bpm needed to randomly accept 0.5 mg(group A1)or 1 mg(group A2)atropine to antagonize(n=10). SNRT, CSNRT, AVN 2∶1 block point and AVNERP were recorded through TELAP. Results Intra-group comparison indicated functional parameters of SN and AVN were inhibited by Dexsat T1. SNRT were prolonged (P<0.05), AVN 2∶1 block point were decreased (P<0.05),AVNERP were prolonged at T1 compared with T0(P<0.05). All indexes in group A1 and AVNERP in group A2 were back to basal level after using atropine at T2(P<0.05). SNRT, CSNRT were shorted at T2 compared with T0 in group A2(P<0.05). AVN 2∶1 block point had more increased at T2 compared with T0 in group A2(P<0.05). Inter-group comparison indicated no significant differences in functional parameters of SN、AVN at T0(P>0.05). SNRT, AVNERP were shorted at T2 in group A2 compared with group A1. AVN 2∶1 block point were increased at T2 in group A2 compared with group A1. Conclusion 0.5 mg atropine may reverse the function of SN and AVN that are inhibited by Dex. 1 mg atropine may increase functions of SN and AVN that are inhibited by Dex.
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