Rishniw M, Tobias A H, Slinker B K
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman 99164-7010, USA.
Am J Vet Res. 1996 Mar;57(3):337-41.
To characterize the magnitude, character, and time course of chronotropic and dysrhythmogenic responses of dogs with vagally mediated bradycardia to atropine sulfate.
Latin square design.
Seven clinically normal adult mixed-breed dogs.
Vagally mediated bradycardia was induced with morphine and fentanyl citrate. Atropine (0.02 mg/kg of body weight) was administered i.v., s.c., or i.m.. Electrocardiograms were recorded continuously for 5 minutes before and for 35 minutes after atropine administration or until a sustained parasympatholytic response was observed. Data were digitized, analyzed independently for changes in atrial and ventricular rate, and compared between different routes of administration.
All dogs developed second-degree atrioventricular (AV) block after i.v. administration of atropine, and 71% of dogs developed AV block after s.c. or i.m. administration. The AV block arose and resolved more rapidly with i.v. administration than with s.c. or i.m. administration. The AV block was principally attributable to an increase in the atrial rate prior to increases in the ventricular rate. Atropine, regardless of route of administration, potentiated baseline ventricular bradycardia in 62% of the experiments (mean heart rate decrease of 16 beats/min; decreased to < 20 beats/min in 2 dogs for < or = 10 seconds). Duration of the bradycardic potentiation was longer with s.c. administration (9.1 minutes, s.c., vs 1.4 minutes, i.v., and 4.6 minutes, i.m.). Parasympatholytic rate was higher for i.v. than s.c. or i.m. administration (128 beats/min vs 92 beats/min and 101 beats/min). Two dogs given atropine s.c. failed to resolve the AV block and attain sinus rhythm.
Administration of 0.02 mg of atropine/kg by i.v., i.m., and s.c. routes for vagally mediated bradycardia in dogs consistently induces AV block and occasional brief potentiation of ventricular bradycardia.
Parasympathomimetic effects occur and resolve most rapidly and consistently, and the stable parasympatholytic effect is of greatest magnitude after i.v. administration. Thus, vagally mediated bradycardia in clinically normal dogs appears to be best abolished by i.v. administration of atropine.
描述迷走神经介导的心动过缓犬对硫酸阿托品变时性和致心律失常反应的程度、特征及时间过程。
拉丁方设计。
7只临床正常的成年杂种犬。
用吗啡和枸橼酸芬太尼诱导迷走神经介导的心动过缓。静脉内、皮下或肌内注射阿托品（0.02mg/kg体重）。在注射阿托品前连续记录心电图5分钟，注射后记录35分钟或直至观察到持续的抗副交感神经反应。数据数字化后，独立分析心房率和心室率的变化，并比较不同给药途径之间的差异。
静脉注射阿托品后所有犬均出现二度房室传导阻滞，皮下或肌内注射后71%的犬出现房室传导阻滞。静脉注射时房室传导阻滞的发生和消失比皮下或肌内注射更快。房室传导阻滞主要归因于心房率在心室率增加之前增加。无论给药途径如何，在62%的实验中阿托品增强了基线心室心动过缓（平均心率降低16次/分钟；2只犬降至<20次/分钟，持续时间≤10秒）。皮下注射时心动过缓增强的持续时间更长（皮下注射9.1分钟，静脉注射1.4分钟，肌内注射4.6分钟）。静脉注射时抗副交感神经率高于皮下或肌内注射（128次/分钟对92次/分钟和101次/分钟）。2只皮下注射阿托品的犬未能解除房室传导阻滞并恢复窦性心律。
对于犬迷走神经介导的心动过缓，静脉内、肌内和皮下注射0.02mg/kg阿托品可一致地诱导房室传导阻滞并偶尔短暂增强心室心动过缓。
拟副交感神经作用出现和消失最快且最一致，静脉注射后稳定的抗副交感神经作用最强。因此，临床正常犬的迷走神经介导的心动过缓似乎最好通过静脉注射阿托品来消除。
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