In 10 anesthetized dogs, we measured high-fidelity left circumflex coronary
(P-LCx), aortic (P-Ao), and left, ventricular (P-LV) pressures and left ci
rcumflex velocity (U-LCx; Doppler) and used wave-intensity analysis (WIA) t
o identify the determinants of P-LCx and U-LCx. Dogs were paced from the ri
ght atrium (control 1) or right ventricle by use of single (control 2) and
then paired pacing to evaluate the effects of left ventricular contraction
on P-LCx and U-LCx. During left ventricular isovolumic contraction, P-LCx e
xceeded P-Ao, paired pacing increasing the difference. Paired pacing increa
sed Delta P-x (the P-LCx-P-Ao difference at the P-Ao-P-LV crossover) and av
erage dP(LCx)/dt (P < 0.0001 for both). During this time, WIA identified a
backward-going compression wave (BCW) that increased P-LCx and decreased U-
LCx; the BCW increased during paired pacing (P < 0.0001). After the aortic
valve opened, the increase in P-Ao caused a forward-going compression wave
that, when it exceeded the BCW, caused U-LCx to increase, despite P-LV and
(presumably) elastance continuing to increase. Thus WIA identifies the cont
ributions of upstream (aortic) and downstream (microcirculatory) effects on
P-LCx and U-LCx.