BLOOD SUPPLY TO THE HEART 1 535 



fig. 7. Reproduction of retraces from an original record taken in a resting unanesthetized dog 

 some days postoperative showing the effect of irreversible hemorrhagic shock on phasic blood pressure 

 and phasic stroke left circumflex coronary flow, using a strain gauge and electromagnetic flowmeter 

 as in fig. 6. A — early; B — midway; C — late in the period of spontaneous hemodynamic decay fol- 

 lowing reinfusion. (L'npublished observations.) 



In the right coronary artery, the contour and time 

 relations of the peripheral coronary pressure curve 

 are similar but the values for systole and diastole and 

 for the cut-off of flow are considerably lower ( 1 53). 



Separation and quantitation of the determinants 

 of coronary flow lying within the myocardial wall, 

 i.e., the vascular and extravascular muscle, are of 

 extreme importance. Various methods have been 

 proposed and used, but they have been only partially 

 successful. The problem of determining the relation- 

 ship of blood flow to active vasomotor changes, 

 irrespective of whether the effect on the intrinsic 

 muscles of the coronary vessels is mediated through 

 the blood stream or is secondary to metabolic changes 

 in the surrounding myocardium, is especially difficult. 

 It is not known how much coronary flow might change 

 with a given change in coronary perfusing pressure 

 without an associated active change in the vasomotor 

 state of the bed. Determination of active variations in 

 vasomotor tone in the coronary bed is further compli- 

 cated by uncontrollable mechanical factors. Varia- 

 tions may occur in the respective durations of systole 

 and diastole during which the rates of flow per unit 

 of time may be quite different and thus obscure any 

 active vasomotor changes. 



By analysis of phasic inflow curves, however, 

 change in the vasomotor state can be separately and 



roughly estimated. A critical point on a coronary 

 inflow curve is selected in late diastole, at which 

 time the rate of change of the volume-elastic and 

 myocardial compression forces is presumed to be 

 minimal (153)- At this point, extravascular forces are 

 at a minimum, the rate of flow reflecting the vaso- 

 motor state of the coronary bed, and the ratio of the 

 aortic pressure to the simultaneously existing rate of 

 flow is then determined. A shift in the diastolic ratio 

 is taken to represent active constriction or dilatation 

 of the coronary bed (41, 146). It has also been sug- 

 gested that change in the extravascular compressing 

 force during systole can be estimated by comparing 

 the diastolic ratio with the ratio of blood pressure to 

 coronary flow at a point in late systole when extra- 

 vascular support is maximal and flow reflects the 

 combined effect of myocardial compression and the 

 existing vasomotor state (146). At this time, the rate of 

 change of the volume-elastic and myocardial com- 

 pression forces is presumed to be minimal. Use of 

 such a systolic point has as yet no experimental 

 verification. 



The problem of determining the magnitude of 

 extravascular support has been approached in differ- 

 ent ways. It has been suggested that intramural 

 pressure can be used as a measure of extravascular 

 compression, and attempts have been made to quanti- 



