1556 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



tion from the right coronary blood. A high degree of 

 coronary dilatation has obviously occurred since 

 right coronary artery flow has increased throughout 

 the cardiac cycle (especially in systole), in the 

 presence of the same or a lower central coronary 

 arterial pressure (153). The mechanisms responsible 

 cannot be identified with certainty. They could be 

 the opening of closed or partially closed capillaries 

 and arterioles, the increased passage of blood through 

 arteriovenous shunts, or increased metabolism. It is 

 probably not explainable on the basis of myocardial 

 hypoxia, since, if the right coronary flow is increased 

 300 to 400 per cent by a constant but very high 

 infusion pressure, the flow increases still further when 

 right ventricular pressure is elevated. Regardless, 

 however, of the mechanism of coronary flow increase, 

 elevation of right ventricular pressure can also be 

 shown to have a flow-reducing effect antagonistic to 

 the flow-promoting mechanisms. In the presence of 

 an adequately maintained central coronary pressure, 

 the sustained flow increase and decrease are preceded 

 and followed by transient periods of flow reduction 

 and elevation. The initial temporary decrease in flow 

 is attributed to the dominant influence of augmented 

 extravascular mechanical compression on the 

 coronary vessels. The subsequent appearance of a 

 sustained increased flow observed shortly thereafter 

 indicates that the effect of coronary dilatation has 

 exceeded the flow reducing effect of increased extra- 

 vascular compression. The immediate and transient 

 flow increase following abrupt lowering of intra- 

 ventricular pressure is a rough index of the extent to 

 which flow had previously been retarded by aug- 

 mentation of extravascular compression. 



Concurrent with the elevation of right coronary 

 flow, left coronary flow and its drainage into the 

 coronary sinus are significantly elevated (153, 196). 

 The increase might be of significant magnitude to be 

 determined in human subjects in the presence of an 

 elevated right ventricular pressure, although this has 

 not been found (312). It might be conjectured that 

 the source of a portion of this increased left coronary 

 blood is increased flow through the ventricular 

 septum, much of which normally drains into the right 

 ventricular cavity but which, because of high right 

 ventricular pressure, might be diverted into the 

 coronary sinus (265). 



Such responses of flow and metabolism in the 

 right myocardium to elevation of its cavity pressure 

 are not peculiar to it. Elevation of left ventricular 

 pressure by an aortic constriction central to the 

 coronary ostia, i.e., between the aortic valves and 

 coronary ostia to stimulate aortic stenosis, gives 



trends for coronary flow and myocardial metabolism 

 of the left ventricle identical to those found in the 

 right ventricle (1 53). 



These maintained changes in the coronary circula- 

 tion could well be the early response in the human 

 being to gradual moderate stenosis of the correspond- 

 ing valves. 



aortic insufficiency. In patients with aortic in- 

 sufficiency and lacking disease of the coronary ostia 

 or arteries, the presence of chest pain resembling that 

 due to myocardial ischemia is generally assigned to a 

 reduction in coronary blood flow, this arising pre- 

 sumably from a reduction of the mean aortic or 

 central coronary diastolic pressure. In the open-chest 

 dog reversible aortic regurgitant flow has been 

 accurately produced without valve injury, metered 

 and controllably varied, while at the same time 

 metering cardiac output. Aortic regurgitant flows in 

 excess of the dog's resting cardiac output resulted in a 

 marked decrease of effective cardiac output, a rise of 

 peripheral resistance and left ventricular end-diastolic 

 pressure, and a marked depression of the left ventricu- 

 lar pressure curve without significant change in mean 

 left atrial pressure. No coronary flows were measured 

 (390). In early experiments in the open-chest dog in 

 rather poor condition (144, 153) reversible aortic 

 insufficiency (umbrella-type aortic valve expanders) 

 sufficient to lower aortic diastolic pressure decreases 

 mean left coronary flow as a resultant of an increased 

 systolic flow and a markedly reduced diastolic flow. 

 On the other hand, Foltz et al. (119), from measure- 

 ments on anesthetized dogs two or three days after 

 the aortic cusps had been torn, found a considerable 

 increase in coronary flow and myocardial oxygen 

 usage. This latter finding has been confirmed by 

 Wegria in acute experiments, and West in chronic 

 dogs (386, 394). In patients with reduced diastolic 

 pressure, wide pulse pressure and varying degrees of 

 left ventricular enlargement, those without angina or 

 failure have normal coronary hemodynamics; those 

 with angina have a reduced coronary flow and cardiac 

 oxygen usage; and those in failure have an increased 

 coronary flow and oxygen usage (constant coronary 

 A-Y oxygen difference) (303). Such observations are 

 difficult to interpret because of their small number, 

 the lack of adequate control data, and the possibility 

 of complicating disease of coronary ostia or arteries, 

 or both. 



mitral stenosis. The general hemodynamic effects 

 from mitral stenosis include increased wedge pressure, 

 pulmonary arterial pressure, right ventricular work, 



