i 54 8 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



coronary inflow (206). It would seem unlikely that 

 the vagus would act as a vasoconstrictor since its 

 chemical transmitter, acetylcholine, is a coronary 

 vasodilator. 



Such studies, of course, do not define the action of 

 the vagi in the intact animal. In the open-chest dog 

 with the heart rate maintained at a constant value 

 by an electric pacemaker, section of these nerves or 

 stimulation of their cut ends does not usually evoke 

 significant change in coronary inflow, coronary 

 sinus flow (orifice meter, bubble flowmeter, rotam- 

 eter), or in coronary A-V oxygen difference, while 

 blood pressure and cardiac output are essentially 

 unchanged (83, go, 236, 339). In all preparations, 

 ventricular contractility is usually not changed (367). 

 These observations are in accord with the apparent 

 lack of vagal fiber distribution to the ventricular 

 myocardium (54, 262). At times, vagal stimulation 

 (378) has been observed to cause reduction in cardiac 

 output, blood pressure, and coronary inflow, an 

 effect which was abolished by atropine. Although 

 this effect is ascribed by the authors to a negative 

 inotropic effect of vagal stimulation on the ventricular 

 muscle, it could also have resulted from diminution of 

 vigor of atrial contraction thus reducing ventricular 

 filling, a finding of different investigators (336). 



sympathetic. Stimulation of the stellate ganglion or 

 its cardiac branches in the anesthetized open-chest 

 dog or in the unanesthetized resting dog increases 

 mean flow in both right and left coronary arteries 

 (83, 139, 153). This augmentation lasts for minutes 

 and persists long after any augmentation of heart 

 rate or blood pressure (if such occurs) has returned 

 to normal. Figure 9 is a response of the left circumflex 

 flow obtained with an electromagnetic flowmeter in a 

 resting unanesthetized dog a few days after probe 

 implantation. In this dog, in which the left stellate 

 ganglion had been previously disconnected from the 

 thoracic sympathetic chain and spinal nerves to 

 eliminate peripheral effects of excitation, stimulation 

 of the common ansa subclavia initially and transiently 

 decreases coronary flow throughout the cardiac cycle 

 without change in blood pressure or heart rate. Within 

 a few seconds, at an unchanged blood pressure but 

 increased heart rate, mean coronary flow increases as 

 the result of an increase in diastolic flow and in spite 

 of a depression of systolic flow with appearance of 

 backflow. Almost immediately, thereafter, coronary 

 flow increases greatly throughout the entire cardiac 

 cycle, with the disappearance of backflow. This 

 pattern of response to stellate stimulation may occur 

 with or without spontaneous elevation of blood pres- 



STELLATE G. STIM. 



RECOVERY 



BLOOD 

 PRESS 



MEAN COR 

 FLOW/MIN 



SYST. COR 

 FLOW/MIN 



MEAN COR. FLOW 

 SYST COR FLOW 



fig. 9. Reproduction of sections from a continuous record in a conscious dog a few days postopera- 

 tive, showing effect of left stellate ganglion stimulation on phasic arterial blood pressure and stroke 

 left circumflex coronary inflow using a strain gauge and electromagnetic flowmeter as in fig. 6. 

 Connections of stellate to sympathetic chain severed at time of operation. [Granata el al. (139).] 



