Kostreva D R, Castaner A, Pedersen D H, Kampine J P
Cardiology. 1981;68(2):65-79. doi: 10.1159/000173266.
Bradycardia was observed during acute cardiac tamponade and severe hemorrhage in pentobarbital-anesthetized morgrel dogs after bilateral cervical vagotomy, sympathectomy and intravenous atropine. An early and a late bradycardia developed during tamponade. A portion of the early bradycardia was produced by a paradoxical increase in vagal efferent nerve activity and a pacemaker shift; however, after vagotomy, sympathectomy and atropine, a significant (p less than 0.02) early and late bradycardia still developed during acute cardiac tamponade and severe hemorrhage. The activation sequence of high and low right atrial electrograms revealed that a pacemaker shift was responsible for the nonvagally mediated bradycardia observed with acute cardiac tamponade and severe hemorrhage. The early and late bradycardias occur with either tamponade or hemorrhage, suggesting that ischemia of the sinoatrial node was the apparent cause of the pacemaker shift and resultant bradycardia.
在双侧颈迷走神经切断术、交感神经切除术并静脉注射阿托品后，对戊巴比妥麻醉的杂种犬进行急性心脏压塞和严重出血时观察到心动过缓。在心脏压塞期间出现了早期和晚期心动过缓。早期心动过缓部分是由迷走神经传出神经活动的反常增加和起搏点移位引起的；然而，在迷走神经切断术、交感神经切除术和阿托品治疗后，急性心脏压塞和严重出血期间仍出现显著（p<0.02）的早期和晚期心动过缓。高低右心房电图的激活序列显示，起搏点移位是急性心脏压塞和严重出血时观察到的非迷走神经介导的心动过缓的原因。早期和晚期心动过缓在心脏压塞或出血时均会出现，提示窦房结缺血是起搏点移位及由此导致心动过缓的明显原因。
