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陈旧性心肌梗死犬运动期间心肌缺血诱发心室颤动的自主神经机制。心脏性猝死的一种实验模型。

Autonomic mechanisms in ventricular fibrillation induced by myocardial ischemia during exercise in dogs with healed myocardial infarction. An experimental preparation for sudden cardiac death.

作者信息

Schwartz P J, Billman G E, Stone H L

出版信息

Circulation. 1984 Apr;69(4):790-800. doi: 10.1161/01.cir.69.4.790.

Abstract

The relationship between activity of the autonomic nervous system, myocardial ischemia, and malignant arrhythmias has been investigated in a new experimental preparation for sudden death. Fifty-seven dogs were chronically instrumented and studied under control conditions (n = 15) and 1 month after production of an anterior myocardial infarction (n = 42). The protocol consisted in occluding the left circumflex coronary artery for 2 min, commencing at the last minute of an exercise stress test and extending through the first minute after cessation of exercise. With this protocol, ventricular fibrillation was observed in 40% of normal dogs and 66% of dogs with infarction. In 14 dogs with infarction, left stellectomy reduced the incidence of ventricular fibrillation to zero (p less than .001). The reflex changes in heart rate elicited within the first minute of ischemia during exercise in the animals that survived (from 204 +/- 14 to 198 +/- 31 beats/min, -6) were opposite those in animals that had ventricular fibrillation (from 208 +/- 24 to 229 +/- 30 beats/min, +21) (p less than .05). The ischemia-induced reduction in heart rate despite continuation of exercise suggests the presence in the dogs that survived of active vagal reflexes that may have played an important role in the maintenance of cardiac electrical stability. This preparation has the potential to induce ventricular fibrillation consistently in conscious animals by the interaction of a few clinically relevant factors (acute myocardial ischemia, submaximal exercise and its cessation, sympathetic and vagal reflexes, and heart rate) and offers the possibility of acquiring further insights into the mechanisms of malignant arrhythmias and evaluating novel strategies for targeted prevention.

摘要

在一种用于研究猝死的新实验模型中,自主神经系统活动、心肌缺血与恶性心律失常之间的关系已得到研究。57只犬被长期植入仪器,在对照条件下(n = 15)以及在前壁心肌梗死形成1个月后(n = 42)进行研究。实验方案包括在运动应激试验的最后1分钟开始,持续2分钟阻断左旋冠状动脉,并延伸至运动停止后的第1分钟。按照此方案,40%的正常犬和66%的梗死犬出现了室颤。在14只梗死犬中,左星状神经节切除术使室颤发生率降至零(p <.001)。存活动物在运动时缺血第1分钟内心率的反射性变化(从204±14次/分钟降至198±31次/分钟,-6)与发生室颤的动物相反(从208±24次/分钟升至229±30次/分钟,+21)(p <.05)。尽管运动仍在继续,但缺血导致心率下降,这表明存活犬存在活跃的迷走反射,这可能在维持心脏电稳定性方面发挥了重要作用。该模型有潜力通过几种临床相关因素(急性心肌缺血、次极量运动及其停止、交感和迷走反射以及心率)的相互作用,在清醒动物中持续诱发室颤,并为深入了解恶性心律失常的机制以及评估针对性预防的新策略提供了可能性。

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