To determine whether reductions in regional myocardial perfusion at reduced coronary arterial pressures reliably indicate maximal vasodilation of the distal vasculature, coronary autoregulation was studied in open-chest dogs at heart rates of -60 beats/min, a level at which metabolic demand, time-averaged systolic compressive forces, and transmural vasodilator reserve approximate those found under usual resting conditions. Circumflex pressure was controlled with a programmable pressure source. Regional circumflex inflow was 0.56 + 0.04(SEM) mlImin-'g-' when circumflex pressure equaled spontaneous aortic pressure and fell to 0.34 + 0.02 ml.min -'g-when circumflex pressure was reduced to 35 mm Hg. Reductions were similar in each myocardial layer, with endocardial flow falling from 0.68 + 0.04 to 0.39 + 0.03 ml-min`.g During adenosine-induced vasodilation at 35 mm Hg, full-thickness and endocardial flows rose to 0.92 + 0.08 and 1.07 ± 0.10 ml.min-'g-', respectively. When coronary pressure was reduced to 25 mm Hg and autoregulation was again operative, full-thickness and endocardial flows fell to 0.28 ± 0.03 and 0.28 ± 0.04 ml min-'g-'. During adenosine vasodilation at 25 mm Hg endocardial flow did not increase significantly but epicardial reserve remained present. These results indicate that significant reductions in regional myocardial perfusion can occur before pharmacologic vasodilator reserve is exhausted. In the absence of tachycardia, endocardial vasodilator reserve can persist to coronary pressures less than 35 mm Hg, but is ordinarily exhausted before epicardial vasodilator reserve.

To quantify reactive elements of the coronary circulation, we have characterized in vivo diastolic coronary input impedance by introducing sinusoidal pressure oscillations of constant amplitude and varying frequency at constant mean pressure levels during prolonged diastoles in heart-blocked dogs anesthetized with pentobarbital. The behavior of coronary input impedance is similar to that observed in other peripheral vascular beds and is a function of both mean distending pressure and vasomotor tone. The behavior of impedance modulus and phase at each pressure level could be described by a lumped resistive-capacitive (RC) parallel model over a frequency range of 1-5 Hz. At higher frequencies the phase angle response could be characterized by adding a Voigt viscoelastic element to the original RC model. Calculated coronary capacitances for both models were similar in magnitude and varied inversely with mean coronary distending pressure. Values for the RC and RC viscoelastic model in the maximally dilated coronary bed were 14.1 and 21.6 X 10(-3) ml X mmHg X 100 g-1 at 30 mmHg and 2.65 and 2.70 X 10(-3) ml X mmHg-1 X 100 g-1 at 110 mmHg. With vasomotor tone intact, calculated coronary capacitance at each pressure level was reduced by a factor of two. These results indicate that an RC parallel model with pressure- and vasomotor tone-dependent capacitance adequately describes diastolic coronary input impedance at frequencies encountered during ordinary diastoles. The addition of a viscoelastic element provides adequate fits up to frequencies of 10 Hz.

The relative contributions of left anterior descending (LAD) and left circumflex (LC) arterial inflow to blood sampled at various points within the great cardiac vein (GCV) and coronary sinus (CS) have been investigated in open-chest dogs. Dissolved helium (He) and hydrogen (H2) were infused into external circuits perfusing the LAD and LC, respectively, and their steady-state concentrations were measured chromatographically at various points within the GCV and CS. Under basal conditions GCV H2 averaged only 5% of mid-CS H2 and did not change greatly during alterations of preload and afterload or during selective LAD or LC obstruction and vasodilation. The relationship of mid-CS He to GCV. He was more variable under basal conditions and changed noticeably during selective changes in LAD or LC inflow. Appreciable amounts of He were present consistently in left marginal vein drainage. We conclude that: 1) GCV blood is remarkably free of LC inflow in both normal and abnormal physiological states; 2) the origin of mid-CS blood is more variable, both from animal to animal and in individual animals before and after interventions; 3) a portion of LAD drainage normally reaches the CS through circumflex venous branches rather than the GCV.

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We examined the "vascular waterfall" hypothesis, which proposes that coronary flow is unaffected by elevations in outflow pressure until the latter reaches a critical threshold level, in 29 isolated canine hearts. In fibrillating hearts vasodilated with adenosine or carbocromen, coronary flow and the coronary pressure-flow relation were not affected by changes in great cardiac vein pressure (PGCV) below a threshold value of 11 +/- 0.9 (mean +/- SEM) mm Hg. Further elevations of PGCV reduced flow and shifted the pressure-flow relation to the right, increasing its pressure-axis intercept (Pf=0). When vasomotor tone was augmented with vasopressin, threshold PGCV increased to 25 +/- 2.7 mm Hg (p less than 0.001). Once again, the pressure-flow relation was unaffected by changes in PGCV below the threshold value and shifted to the right when this value was exceeded. The amount by which spontaneous values of Pf=0 exceeded threshold values of PGCV was greater when vasomotor tone was augmented than during vasodilation. Pf=0 continued to exceed PGCV when the latter was raised above the threshold level. Both Pf=0 and threshold values of PGCV were less during a long diastole than during ventricular fibrillation. We reached the following conclusions. 1) During changes in PGCV below a threshold value, the coronary circulation exhibits traditional waterfall behavior. 2) The threshold pressure for altering waterfall behavior is affected by vascular tone and mechanical activity. 3) Pf=0 remains above PGCV when the latter is increased above the threshold value needed to alter flow.