Direct activation of cardiac adrenergic nerve endings by defibrillator shocks.
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.
D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004554:Electric Countershock; D006321:Heart / Q000294:innervation* / Q000502:physiology; D066298:In Vitro Techniques