Key result
Increases in perfusate flow evoked venular dilations up to 36 ± 9 μm, which were significantly reduced by L-NNA and converted to constriction by the addition of indomethacin.
Population
Pressurized (10 mmHg) and norepinephrine-preconstricted skeletal muscle venules (179 +/- 8 micron in diameter)
Comparison
Increases in perfusate flow before and after… vs Baseline conditions
Design
Preclinical
Authors
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Hypothesis-generating for venular shear stress regulation in skeletal muscle; leaves open translation to human microcirculation.
In skeletal muscle venules, increased shear stress from perfusate flow stimulates endothelium-derived NO and prostaglandins to elicit dilation, regulating wall shear stress.
Koller et al. (1998) studied this question. Increases in perfusate flow vs. Endothelium removal, L-NNA, and indomethacin was evaluated on Changes in diameter of pressurized and norepinephrine-preconstricted venules. Increases in perfusate flow evoked venular dilations up to 36 ± 9 μm, which were significantly reduced by L-NNA and converted to constriction by the addition of indomethacin.
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