Niebauer M J, Geddes L A, Babbs C F
Med Instrum. 1986 May-Jun;20(3):162-3.
Defibrillator shocks ranging in intensity from three to nine times current threshold were delivered to four isolated, metabolically supported, beating canine hearts. The shocks produced an immediate, current-dependent depression of left ventricular isovolumic systolic pressure. This depression was transient, reproducible, and was followed by a transient overshoot in ventricular systolic pressure. Then 1 mg propranolol hydrochloride in 1 ml H2O was injected into the coronary arterial supply of the isolated heart, and the shocks were repeated. The magnitude of the immediate cardiac depression after shock was unchanged; however, the time required for full recovery of left ventricular systolic pressure to a pre-shock control value was prolonged. In addition, the transient overshoot in ventricular systolic pressure seen in the untreated state was absent. These results are consistent with the hypothesis that defibrillatory shocks produce a direct activation of cardiac adrenergic nerves, which aid in recovery of ventricular contractility following defibrillator shocks.
将强度为电流阈值三至九倍的除颤电击施加于四颗离体的、有代谢支持的、正在跳动的犬类心脏。电击导致左心室等容收缩压立即出现与电流相关的下降。这种下降是短暂的、可重复的，随后心室收缩压会出现短暂的超调。然后将1毫克盐酸普萘洛尔溶于1毫升水中注入离体心脏的冠状动脉供血中，再次进行电击。电击后立即出现的心脏抑制程度没有变化；然而，左心室收缩压完全恢复到电击前对照值所需的时间延长了。此外，在未处理状态下观察到的心室收缩压短暂超调消失了。这些结果与以下假设一致：除颤电击直接激活心脏肾上腺素能神经，这有助于除颤电击后心室收缩力的恢复。
