NEURAL FACTORS AFFECTING CARDIAC ARRHYTHMIAS INDUCED BY HALOPROPANE

¹ Department of Anesthesiology and Department of Pharmacology, Columbia University, College of Physicians and Surgeons and the Anesthesiology Service, The Presbyterian Hospital, New York, New York

Cardiac arrhythmias were produced in the cat by the inhalation of: 1) halopropane (1-2%), 2) halopropane (1%) + 10% carbon dioxide; 3) halopropane (1%) + 1 µg/kg epinephrine intravenously. The halopropane arrhythmia was abolished by decerebration, spinal cord transection, Hydergine (10-20 µg/kg) or pretreatment with reserpine (0.1 mg/kg i.p. for 1 day), but not by vagotomy, atropine (2 mg/kg) or ethybenztropine (0.1-02 mg/kg). The halopropane-carbon dioxide arrhythmia was abolished by spinal cord transection, by a combination of reserpine pretreatment (1 day) plus acute bilateral adrenalectomy or by reserpine pretreatment (7 days), but not by vagotomy, atropine, decerebration, Hydergine, acute bilateral adrenalectomy or reserpine pretreatment (1 day). The halopropane-epinephrine arryhthmia was not abolished by vagotomy, atropine, decerebration, spinal cord transection or reserpine (7 days). It was concluded that the presence of suprapontine structures was necessary for the halopropane arrhythmia, while the halopropane-carbon dioxide arrhythmia required an intact pons and medulla. The halopropane-epinephrine arrhythmia did not require the presence of any of these structures. Although parasympathetic nervous system blocking agents and vagotomy did not affect the three arrhythmias, the sympathetic nervous system and/or catecholamines had an important role in the genesis of these arrhythmias.