(Circulation. 1999;100:1555-1561.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Regulation of Shear Stress in the Canine Coronary Microcirculation
From the Department of Physiology, Medical College of Wisconsin, Milwaukee.
Correspondence to David W. Stepp, PhD, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail dstepp{at}post.its.mcw.edu
Background—Physical forces, such
as pressure and flow, are well known to affect vascular function in the
coronary circulation. Increases in shear stress produce
vasodilation in coronary arterioles in vitro, and constant-flow
preparations suggest a role for shear stress–induced vasodilation
during adjustments to metabolic demand in vivo.
Hypothetically, the regulation of shear stress can be viewed as a
negative feedback control scheme (increased velocity 
increased
shear vasodilation decreased velocity shear normalized).
Therefore, we hypothesized that shear stress would be at least
partially regulated during conditions of elevated flow.
Methods and Results—We used fluorescence microangiography to measure microvascular diameters and velocities in the coronary circulation in vivo and used these variables to calculate shear stress. Measurements were obtained under basal conditions, during maximal coronary blood flow, and after inhibition of NO synthase. Basal shear stress in the coronary circulation averaged 10 dyn/cm2 in small arteries and 19 dyn/cm2 in arterioles. Regulation of shear stress was observed in small arteries during adenosine-induced increases in coronary blood flow, but arterioles showed minimal regulation. NO synthase blockade had no effect on basal shear stress but completely abolished its regulation in small arteries during vasodilation.
Conclusions—Our data provide the first quantitative estimates of microvascular shear stress in the coronary circulation. Moreover, our results suggest that shear stress in small coronary arteries is regulated by NO release from the endothelium.
Key Words: stress • circulation • nitric oxide synthase
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