

HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



tized dog with a chronically implanted electromag- 

 netic flowmeter on the coronary artery. 



To the author's knowledge, the existence of a 

 tonic action on the coronary circulation of the intact 

 animal, attributable to the parasympathetic and 

 sympathetic nerve fibers, has never been demon- 

 strated, the section of these nerves in the open-chest 

 dog leading only to nonspecific changes. Study of this 

 problem should be made through the application to 

 the coronary circulation of recent techniques for 

 coronary neurectomy and extrinsic cardiac denerva- 

 tion on chronic dogs (43, 71). 



reflex control. Our knowledge of the role of the 

 central nervous system in regulation of the coronary 

 circulation in health and disease is sufficient to war- 

 rant discussion but is certainly insufficient to draw 

 firm conclusions. This arises from a lack of proper 

 experiments in which studies of both the reflexes and 

 the coronary hemodynamic responses have been 

 simultaneously made. A proper demonstration de- 

 pends on the observations that the vagus and sym- 

 pathetic nerves to the heart are tonically active as 

 far as coronary blood flow regulation is concerned, or 

 can be made so by the induction of adequate stimuli 

 arising either within the heart or peripherally. 



Different observations support the view that there 

 are receptors in the distribution of the canine left 

 coronary artery. Injection of veratridine into a left 

 coronary artery (but not the right coronary), going 

 only to the left ventricular muscle and in amounts 

 insufficient to affect the systemic circulation upon 

 direct injection into the left ventricle, causes an 

 abrupt fall in blood pressure and heart rate (76, 77). 

 ( lirculatory depression which may follow selective 

 augmentation of central coronary pressure near the 

 left coronary orifice and the initial part of the cle- 

 scendens artery, or which may occur during coronary 

 sinus occlusion, is relieved by vagal section (132, 187, 



285). 



The evidence is equivocal that flow in one coronary 

 artery can be influenced reflexively and adversely by 

 impulses arising in another occluded coronary artery. 

 Various supportive observations suggest that noxious 

 intercoronary reflexes can be made to occur: a) 

 Ligation of a coronary artery is stated to cause reflex 

 spasm or vasoconstriction in the other coronary artery 

 resulting in fatal ventricular fibrillation (231). This 

 is presumed to be abolished by bilateral vagosym- 

 pathetic blockade (228). The infarction after coronary 

 ligation is increased with vagal stimulation and is 

 prevented by local anesthesia of the vessel wall at the 



site of the ligature (220, 223). b) In the anesthetized 

 closed-chest dog with visualization of the coronary 

 artery bed by cinefluorography after injection of a 

 radiopaque dye, selective embolization (lycopodium 

 spores) of a coronary artery branch results in a marked 

 decrease in size of the nonembolized coronary artery 

 bed and in coronary sinus flow (165). On the other 

 hand, a) West et al. (392), using techniques similar to 

 those of Guzman, failed to find evidence of reflex 

 coronary vasoconstriction following coronary em- 

 bolization. /)) In the open-chest dog, following liga- 

 tion of the right or left coronary artery, the coronary 

 flow (rotameter) rises and resistance falls in the un- 

 occluded coronary artery, such flow augmentation 

 presumably resulting from an anatomical and func- 

 tional overlap of the right and left coronary arteries 

 (153, 282, 377). c) In the unanesthetized resting dog, 

 some days after implantation of an electromagnetic 

 flowmeter on the main left coronary artery or a major 

 arterial branch, temporary (10-30 sec) occlusion of a 

 left coronary artery branch results either in no change 

 or an increase in blood flow in the artery in which 

 flow is being measured ( L. C. Fisher, unpublished obser- 

 vations). It must be remembered that these experiments 

 with negative results follow considerable dissection of 

 the coronary arteries, and actually represent con- 

 ditions which deviate extensively from the normal 

 nerve state. Thus they do not rule out the possibility 

 of reflex coronary vasoconstriction occurring in small 

 localized regions of the myocardium after coronary 

 occlusion. 



Changes in coronary blood flow which might result 

 from extracardiac stimuli would be of great clinical 

 interest, and their demonstration might aid in eluci- 

 dating the mechanism of the relationship between 

 angina pectoris and its various incitants, such as 

 eating, abdominal distention, cold, and exercise. The 

 claim is made that many diverse afferent stimuli affect 

 the coronary circulation. Prolonged experimental 

 neurosis in monkeys produced by conflicting condi- 

 tioned reflexes or selected brain stimulation can pro- 

 duce ECG changes identical to those of human 

 ventricular ischemia (250). Stimulation of many 

 afferent nerves, distention of the stomach, gall bladder 

 and esophagus, and cutaneous pain, all are presumed 

 to decrease coronary flow in the anesthetized dog, 

 while elevation of cerebral blood pressure and carotid 

 sinus pressure decreases coronary flow in the inner- 

 vated heart-lung preparation (blood pressure and 

 heart rate kept constant) (153). In these experiments, 

 the recording devices and data were generally in- 

 sufficient to establish that no changes occurred in 



