Key result
Elevated coronary perfusion pressure redistributes flow toward the subendocardium, signaling earlier subendocardial autoregulatory failure.
Why the study?
The transmural variation in coronary autoregulatory response to elevated perfusion pressure in hyperperfused myocardium was not well characterized.
p-value: p=<0.05
In a canine model, the subepicardial vasculature appears better adapted to autoregulate blood flow at elevated perfusion pressures compared to the subendocardium.
Highlights limits of transmural autoregulation at extreme pressures in dogs; leaves open translation to clinical hypertension.
We assessed transmurally the coronary autoregulatory response to elevated perfusion pressure in 85 anesthetized, open-chest dogs.Steady state and transient flow distributions were measured with 9 ± 1 /im 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) mm Hg, whereas Endo:Epi 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 first in subendocardium.At high perfusion pressures, subendocardial flow exceeded subepicardial flow (P < 0.05) whether 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 minutes this ratio had returned to near control.In contrast, 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 oxygen demand could not explain greater subendocardial flow since (1) elevated perfusion pressure had no effect on aortic and left ventricular pressures, cardiac output, and heart rate, (2) left ventricular oxygen consumption was constant in the presence of preferential subendocardial perfusion, (3) regional myocardial oxygen tension increased in parallel with blood flow to subepicardium and subendocardium.Also, elevated perfusion pressure caused a greater steady state increase in subendocardial flow in four empty, nonworking hearts.The results demonstrate transmural variation in coronary autoregulatory potential; the subepicardial vasculature appears better adapted to autoregulate blood flow at elevated perfusion pressures.
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Boatwright et al. (1980) studied Coronary autoregulation in hyperperfused myocardium (n=85). Elevated perfusion pressure vs. Normal/control perfusion pressure was evaluated on Transmural coronary blood flow distribution (Endo:Epi ratio) (p=<0.05). Elevated coronary perfusion pressure caused progressive redistribution of flow toward the subendocardium, indicating that autoregulation fails first in the subendocardium (P<0.05).
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