Regulation of shear stress in the canine coronary microcirculation

Citation
Dw. Stepp et al., Regulation of shear stress in the canine coronary microcirculation, CIRCULATION, 100(14), 1999, pp. 1555-1561
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
100
Issue
14
Year of publication
1999
Pages
1555 - 1561
Database
ISI
SICI code
0009-7322(19991005)100:14<1555:ROSSIT>2.0.ZU;2-P
Abstract
Background-Physical forces, such as pressure and flow, are well known to af fect vascular function in the coronary circulation. Increases in shear stre ss produce vasodilation in coronary arterioles in vitro, and constant-flow preparations suggest a role for sheer stress-induced vasodilation during ad justments to metabolic demand in vivo. Hypothetically, the regulation of sh ear stress can be viewed as a negative feedback control scheme (increased v elocity --> increased shear --> vasodilation --> decreased velocity --> she ar normalized). Therefore, we hypothesized that shear stress would be at le ast partially regulated during conditions of elevated flow. Methods and Results-We used fluorescence microangiography to measure microv ascular diameters and velocities in the coronary circulation in vivo and us ed these variables to calculate shear stress. Measurements were obtained un der basal conditions, during maximal coronary blood flow, and after inhibit ion of NO synthase. Basal shear stress in the coronary circulation averaged 10 dyn/cm(2) in small arteries and 19 dyn/cm(2) in arterioles. Regulation of shear stress was observed in small arteries during adenosine-induced inc reases in coronary blood flow, but arterioles showed minimal regulation. NO synthase blockade had no effect on basal shear stress but completely aboli shed its regulation in small arteries during vasodilation. Conclusions-Our data provide the first quantitative estimates of microvascu lar shear stress in the coronary circulation. Moreover, our results suggest that shear stress in small coronary arteries is regulated by NO release fr om the endothelium.