Mechanism of cardiac arrhythmias induced by diencephalic stimulation

¹ Department of Pharmacology and Physiology, Emory University School of Medicine, Atlanta, Georgia

Electrical stimulation of numerous areas in the midbrain reticular formation and in the posterior hypothalamus of the cat increased blood pressure and caused a variety of electrocardiographic changes, including sinus tachycardia, ventricular premature contractions, bigeminal rhythm, A-V dissociation, and ventricular tachycardia. Most commonly, these arrhythmias developed immediately after cessation of diencephalic stimulation but also developed during the period of stimulation in 5 of the 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The arrhythmias also were abolished by methylscopolamine, by bilateral vagotomy, or by extirpation of the stellate ganglia. Electrical stimulation of the distal end of the cut right vagus nerve slowed the sinus rate and electrical stimulation of the right stellate ganglion elevated sinus rate, but neither of these procedures caused arrhythmias. Simultaneous stimulation of both the right vagus nerve and the right stellate ganglion, however, caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by diencephalic stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart.

Note:
With the Collaboration of W. N. Kelly and C. E. Johnson

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