BLOOD SUPPLY TO THE HEART 



'549 



sure and heart rate, or when the aortic blood pressure 

 (in open-chest dogs) is artificially controlled and 

 compensated to the control level. This indicates that 

 the factors of heart rate, blood pressure, and work 

 are not indispensable to the natural mechanism 

 through which the flow increase is mediated. The 

 major portion of the flow increase is related to acti\<- 

 dilatation since blood pressure does not necessarily 

 rise. The net flow increase rests in part, however, on a 

 mechanical basis, for the duration of systole (in which 

 flow is less than in diastole) is reduced and thus, at 

 the same heart rate, the period of time occupied by 

 diastole (in which rate of flow is greater), is increased 

 considerably. About 30 per cent of the flow increase 

 is estimated to be due to this shortening of systolic 

 and lengthening of diastolic time per beat or per 

 minute (93). Concurrently, left ventricular oxygen 

 usage, cardiac output, and cardiac work, either per 

 minute or per heart beat, increase while the systolic 

 and diastolic dimensions of the heart decrease. Since 

 the blood pressure and heart rate do not necessarily 

 change during the flow increase, while duration of 

 systole shortens, the stroke coronary flow does not 

 correlate with pressures developed by the ventricle 

 or with directional trends in ventricular tension 

 calculated thereon. 



The evidence is well founded that stimulation of the 

 sympathetic nerves to the heart aids greatly in main- 

 taining and augmenting the rate and contractility of 

 the heart, as shown by improvement in the atrial and 

 ventricular function curves from any given atrial, 

 ventricular end-diastolic pressure (263, 336), or fiber 

 length, and in the gradient of the aortic pressure and 

 stroke volume curves (11, 153, 211). In no experiment 

 has coronary inflow been found to increase without 

 experimental evidence of increased vigor of contrac- 

 tion, increased cardiac work, and metabolism. The 

 mechanism by which this is accomplished has not 

 been completely identified. The possibility that 

 adrenal secretion is responsible for the cardiac stimu- 

 lating effect has been largely discounted experi- 

 mentally (153)- The facts that a) administration of 

 acetylcholine to an atropinized heart results in libera- 

 tion of an adrenaline-like substance (186); /;) that 

 this substance is also normally present in heart ex- 

 tracts (376); and c) that stimulation of cardiogenic 

 sympathetic fibers sets free an adrenaline-like sub- 

 stance (284, 346), all support the view that a dominant 

 role is played by myocardial catecholamines. 



The experiments of Eckstein et al. (93) offer evi- 

 dence that this process is very wasteful, for the increase 

 in the work of the heart is not essential to the asso- 



ciated increase in coronary inflow. Stimulation of the 

 accelerator nerves in the open-chest dog produces an 

 increase in vigor of contraction, cardiac output, 

 cardiac work, coronary blood flow, and oxygen con- 

 sumption. However, simultaneous nerve stimulation 

 and inflation of a left auricular balloon to reduce the 

 external work of the heart below the control value is 

 likewise followed by increased vigor of contraction, 

 increased coronary flow and increased oxygen con- 

 sumption. Thus, the adrenaline-like substance re- 

 leased by nerve stimulation would appear to increase 

 oxygen consumption directly. 



The preceding observations do not preclude the 

 possibility that the major influence of the sympathetic 

 cardiac nerves may be to exert a direct vasomotor 

 influence on the coronary vessels, the initial temporary 

 coronary vasoconstriction which invariably occurs 

 being overpowered by metabolic dilator influences 

 associated with the type of stimulation. It is, however, 

 most difficult to establish and identify conclusively, 

 by experimental means, the separate effects of nervous 

 influences upon the myocardium and coronary vessels 

 because the physiological functions of these structures 

 are so intimately related that their individual re- 

 sponses can be secondarily modified, each by the 

 other. In the innervated fibrillating heart, stellate 

 stimulation at times decreases coronary flow, while 

 nerve section increases coronary flow (206). Recent 

 evidence indicates the existence and functional im- 

 portance of coronary vasomotor fibers the action of 

 which in previous investigations was presumably 

 obscured because of a nonselective type of nerve 

 stimulation (199, 358). As other workers have shown, 

 excitation of high threshold postganglionic (stellate 

 or inferior cervical) cardiosympathetic fibers with 

 high voltage and high frequency stimulation causes 

 profound alterations in myocardial metabolism which 

 could not be prevented by ergotamine or atropine. 

 However, appropriate stimulation of preganglionic 

 fibers, using low voltage and low frequency, leads 

 either to coronary vasoconstriction (decreased coro- 

 nary flow and blood pressure and increased coronary 

 A-V oxygen without alteration in oxygen consump- 

 tion), or to coronary vasodilation (increased coronary 

 flow, decreased coronary A-V oxygen without blood 

 pressure elevation and without alteration in cardiac 

 metabolism). The magnitude and importance of these 

 direct vasomotor effects remain to be determined. 

 In the author's laboratory, preliminary attempts have 

 failed to demonstrate these direct vasomotor influences 

 of the cardiac sympathetic fibers in the unanesthe- 



