BLOOD SUPPLY TO THE HEART 



1569 



of occlusion (by ligation) of a left coronary artery 

 branch is considerable, being about 30 20 mm Hg, 

 and the central coronary resistance is quite low (153). 

 The effect of a central constriction on coronary flow 

 is a function of how much the resistance imposed by- 

 it is in relation to the resistance in the coronary bed. 

 When the flow to the bed is reduced by central 

 constriction, the peripheral vessels dilate as a result 

 of the associated ischemia and the flow may tend to 

 increase, the combined result of which will be a new 

 equilibrium. Hence, since the peripheral resistance in 

 the coronary bed is constantly changing and will be 

 decreased by the anoxia induced by the central 

 constriction, and since the effect on flow of any central 

 constriction of lumen is a function of how much that 

 resistance is, in relation to peripheral resistance, no 

 predictions can be made as to the effect on blood 

 flow when the coronary artery is constricted by known 

 amounts. Since the peripheral resistance is relatively 

 high, generally sizeable reductions in lumen are 

 necessary before inflow decreases. Thus, the reduction 

 of lumen of a coronary vessel may be of little func- 

 tional importance to the vascular bed supplied by 

 that vessel when the rate of flow is normal or some- 

 what low, but the same constriction can seriously 

 limit flow to the same bed just at the time when the 

 requirements of the latter are greatest and flow would 

 otherwise be much greater (153). Obviously, how- 

 ever, this compensatory dilatation of the coronary bed 

 in the presence of constriction of its central coronary 

 artery has a limit, and flow through it will ultimately 

 fall significantly. In part because of this, the heart 

 has a remarkable ability to retain viability of its 

 muscle beyond a constriction, and significant changes 

 in the electrocardiogram do not occur until coronary 

 inflow is reduced approximately 70 per cent (383). 



Studies have been made of how quickly such an 

 ischemic area with its potential collateral supply of 

 oxygen becomes nonviable. Admittedly, tests for 

 viability are crude. However, if the criteria used are 

 an absence of local action currents, failure of local 

 conduction, and lack of movement in the presence of 

 generalized ventricular fibrillation, then viability 

 does not usually continue beyond an hour, although 

 occasionally the presence of local action currents and 

 excitability may persist from 2 l 2 to 7 hours (403). 

 The return of normal myocardial function has been 

 studied also after reinstitution of coronary flow in dog 

 hearts maintained anoxic for prolonged periods on an 

 extracorporeal circulation. Hearts maintained anoxic 

 for up to 100 min can maintain their blood pressure 

 on removal from the extracorporeal circulation (65). 



Within 1 min after occlusion of a left coronary 

 artery branch, the intracoronary pressure beyond this 

 point drops to about 30 20 mm Hg and useful 

 function is lost, for the muscle now lengthens during 

 systole of the left ventricle (359). When, however, 

 the peripheral end of this ligated coronary artery is 

 permitted to bleed externally, collateral arterial 

 blood appears immediately, averaging about 3.0 ml 

 per min for about 50 g of potentially infarcted myo- 

 cardium, and this blood can be shown to come from 

 the other nonoccluded coronary arteries (153). The 

 collateral communications are largely in the epicardial 

 areas (40). Probably not more than 2.4 ml of this 

 blood (containing 0.5 ml oxygen) would perfuse the 

 myocardial bed if the collateral flow were not per- 

 mitted to bleed externally. This is because of the 

 peripheral resistance existing beyond the point of 

 occlusion and averaging 20 or so mm Hg. That most 

 of this calculated collateral flow actually traverses 

 the capillary bed is evidenced by the fact that the 

 electrocardiogram improves when the collateral flow 

 is not permitted to bleed externally (96, g8). 



Most of these hearts with occlusion of a major left 

 coronary artery branch die within a number of 

 hours. For example, experimental ligation of the left 

 circumflex coronary artery may give mortalities of 

 70 per cent or more (170). Other hearts are more 

 fortunate, for if they survive the first few hours, then, 

 for some completely unknown reason, within 12 

 hours collateral flow starts to rise, doubling within 2 

 days, and within 3 to 4 weeks it may approximate 40 

 to 100 per cent of normal inflow into that coronary 

 artery. Almost all the collateral flow comes from the 

 unoccluded coronary arteries. The myocardial fibers 

 which were lengthening early after occlusion now 

 shorten in systole. Concurrently, the peripheral 

 coronary pressure increases to values somewhat less 

 than the normal central coronary pressure and the 

 myocardium shortens during systole (153). 



MEANS OF EXPERIMENTALLY CHANGING COLLATERAL 

 FLOW EARLY AFTER CORONARY OCCLUSION. The level 



of collateral flow with its oxygen content is estimated 

 to be about 40 per cent of that calculated as necessary 

 to maintain indefinitely the viability of this myo- 

 cardium, since the oxygen uptake of 50 g of a heart 

 with perfused coronary arteries at rest and doing no 

 external work approximates 1.2 ml, as compared to 

 the immediately available collateral oxygen supply of 

 0.5 ml (249). Hence, it is important to try to increase 

 immediately this collateral flow or backflow. Except 

 for one report on the positive effect of nitroglycerin 



