Circulation, Vol 71, 370-377, Copyright © 1985 by American Heart Association
JM Canty Jr and FJ Klocke
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 approximately 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) ml . min-1 . g-1 when
circumflex pressure equaled spontaneous aortic pressure and fell to 0.34
+/- 0.02 ml . min- 1 . g-1 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-1 . g-1. 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-1 . g-1,
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-1 . g-1. 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.
ARTICLES
Reduced regional myocardial perfusion in the presence of pharmacologic vasodilator reserve
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