W. p. GEIS AND M. P. KAYE 
299 
BP 
mmHg 
200 
CONTROL 
100 
oL 
LT. CERVICAL VAGUS 
LT. SVC RT. SVC LT. PA 
^^^^ A% >ii||[|||||||^ji|||[ | | iiiiiiiin ^ 
RAF 
BE(RA) 
LAF 
RVF -/"^-JMiliiLXx 
BE(RV) 
109 154 
n' i h 
154 154 
154 154 
154 
Figure 3. — Regional Denervation of the Canine Heart. 
Lt. cervical vagus stimulation 
BP = blood pressure; 
RAF=rt. atrial contractile force 
BE (RA) =bipolar electrogram, rt. atrium 
LAFr^lt. atrial contractile force 
RVF=rt. ventricular contractile force 
BE (RV) =bipoIar electrogram, rt. ventricle 
remaining nerves did not result in augmenta- 
tion of contractility in either atria. 
Right Atrium 
On all occasions, augmentation of RA con- 
tractility due to stimulation of the right stel- 
late cardiac nerve was interrupted by transec- 
tion of the SVC. Innominate nerve or recurrent 
cardiac nerve augmentation of RA was inter- 
rupted on all occasions by transection of the 
medial SVC or transection of the superior LA. 
Interruption of augmentation of the RA during 
stimulation of the VMCN and VLCN was 
accomplished by either transection of the 
medial SVC or by interruption of nerves along 
the root of the great vessels. Only rarely did 
a single intervention interrupt the positive 
inotropic response to stimulation of the right 
anterior ansa, the right posterior ansa, the 
left anterior ansa and the left posterior ansa. 
The magnitude of inotropic response to each of 
these nerves was usually depressed after any 
one of the following interventions : transection 
of the SVC, transection of the superior LA, or 
interruption of nerves along the root of the 
great vessels. However, following all three of 
the named procedures, interruption of augmen- 
