I t is generally accepted that excitation of the sympathetic innervation of the heart significantly alters myocardial excitability, conductivity and contractility. Actual experimental demonstration of each of these properties has occurred only within relatively recent years although the influence of the catecholamines has been known. Marked alterations in the rate of rise of ventricular systolic pressure and the rate of fall of diastolic pressure have led to the deduction that sympathetic excitation exerts an important influence on the synchrony of myocardial contraction ( 1,2 ) . While recording pressure simultaneously from both ventricles, it became obvious to us that the pressure elevations in the ventricles early in systole were asynchronous. During stellate stimulation, however, these pressure elevations became more nearly simultaneous. The present report describes this synchronization of contraction of the two ventricles as a result of stellate stimulation.Methods. Pressures were recorded simultaneously from the 2 heart chambers of the dog as previously described( 1). An Offner Type R Dynograph was employed as the recording instrument. Through the widely opened chest, cannulae were introduced into each of the ventricular chambers and the Statham transducers adjusted to chamber level to insure accurate zero recordings. The animals were anesthetized with Sernylant (2 mg/kg) followed by i.v. chloralose (80 mg/ kg). Both stellate ganglia were prepared for stimulation by means of bipolar electrodes and a Grass model S 5 stimulator set to deliver square-wave pulses at 5 msec., 10/sec. and 4-5 volts. Stimulation pulses were monitored by an oscilloscope across the stimulating electrodes. Records were made at 2.5, 25 *Supported by a grant from NIH. t The Sernylan was generously furnished by Parke, Davis and Co. and 250 mm/sec., the latter being employed in precise measurement of time intervals. Positive pressure respiration was maintained by means of a Harvard respirator. Standard limb leads of the ECG were recorded and stellate ganglion stimulation repeated several times from each side, both before and after bilateral vago tomy.ResuZts. Fig. 1 shows simultaneously recorded pressure pulses from both the right and left ventricles together with the ECG, before (A), immediately after cessation of electrical excitation of the left stellate ganglion ( B ) and following 2 minutes recovery time (C). Brief segments of the traces recorded at 25 mm/sec are followed by pulses recorded a t 250 mm/sec in each instance. Although small presystolic pressure waves were associated with the a-wave of atrial contraction in each of the ventricles, the point of initial rise in intraventricular pressure is clear. I t is evident that pressure A