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1 Departments of Medicine and Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and 2 Physiological Flow Studies Group, Department of Biological and Medical Systems, Imperial College of Science, Technology, and Medicine, London SW7 2BY, United Kingdom
In 10 anesthetized dogs, we measured high-fidelity left
circumflex coronary (PLCx), aortic (PAo), and
left ventricular (PLV) pressures and left circumflex
velocity (ULCx; Doppler) and used wave-intensity
analysis (WIA) to identify the determinants of PLCx and
ULCx. Dogs were paced from the right 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 PLCx and
ULCx. During left ventricular isovolumic
contraction, PLCx exceeded PAo, paired pacing
increasing the difference. Paired pacing increased 
PX
(the PLCx-PAo difference at the
PAo-PLV crossover) and average
dPLCx/dt (P < 0.0001 for both).
During this time, WIA identified a backward-going compression wave
(BCW) that increased PLCx and decreased
ULCx; the BCW increased during paired pacing (P < 0.0001). After the aortic valve opened, the
increase in PAo caused a forward-going compression wave
that, when it exceeded the BCW, caused ULCx to
increase, despite PLV and (presumably) elastance continuing
to increase. Thus WIA identifies the contributions of upstream (aortic)
and downstream (microcirculatory) effects on PLCx and
ULCx.
coronary blood flow; hemodynamics; contraction; relaxation
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