Transmural variation in autoregulation of coronary blood flow in hyperperfused canine myocardium.

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Abstract
The coronary autoregulatory response to elevated perfusion pressure was assessed transmurally in 85 anesthetized, open-chest dogs. Steady state and transient flow distributions were measured with 9 .+-. 1 .mu.m radioactive microspheres. Steady state distributions of myocardial blood flow were uniform transmurally (P > 0.05) at perfusion pressures of 103 .+-. 1 (n = 81) and 146 .+-. 2 (n = 34) mmg Hg; endo:epi [endocardial:epicardial] ratios of 1.26 .+-. 0.05 and 1.51 .+-. 0.07 at perfusion pressures of 194 .+-. 1 (n = 60) and 221 .+-. 3 (n = 14) mm Hg, respectively, indicated progressive redistribution (P < 0.05) of flow toward subendocardium. As perfusion pressure was increased, autoregulation failed 1st in subendocardium. At high perfusion pressures subendocardial flow exceeded subepicardial flow (P < 0.05) where or not subepicardial flow was autoregulated. The initial, transient response to elevation of coronary perfusion pressure from 99 .+-. 1 to 145 .+-. 2 (n = 5) mm Hg was an increase (P < 0.05) in endo:epi ratio from 1.05 .+-. 0.06 to 1.30 .+-. 0.06. By 2 min this ratio returned to near control. The initial endo:epi ratio of 1.32 .+-. 0.05 caused by elevation of perfusion pressure to 190 .+-. 5 (n = 6) mm Hg did not wane (P > 0.05). A selective increase in subendocardial O2 demand could not explain greater subendocardial flow since elevated perfusion pressure had no effect on aortic and left ventricular pressures, cardiac output and heart rate; left ventricular O2 consumption was constant in the presence of preferential subendocardial perfusion; and regional myocardial O2 tension increased in parallel with blood flow to subepicardium and subendocardium. Elevated perfusion pressure caused a greater steady state increase in subendocardial flow in 4 empty, nonworking hearts. Transmural variation in coronary autoregulatory potential was demonstrated; the subepicardial vasculature appears better adapted to autoregulate blood flow at elevated perfusion pressures.