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1 Department of Medical Engineering, Kawasaki Medical School, Kurashiki, Okayama, Japan
2 Department of Medical Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
* To whom correspondence should be addressed. E-mail: mochi{at}me.kawasaki-m.ac.jp.
Endothelium-derived nitric oxide (NO) is synthesized in response to chemical and physiological stimuli. Here, we investigated a possible role of the endothelial cell glycocalyx as a biomechanical sensor that triggers endothelial NO production by transmitting flow-related shear forces to the endothelial membrane. Isolated canine femoral arteries were perfused with a Krebs-Henseleit solution at a wide range of perfusion rates with and without pretreatment by hyaluronidase to degrade hyaluronic acid glycosaminoglycans within the glycocalyx layer. NO production rate was evaluated as the product of nitrite concentration in the perfusate and steady-state perfusion rate. The slope that correlates the linear relation between perfusion rate and NO production rate was taken as a measure for flow-induced NO production. Hyaluronidase treatment significantly decreased flow-induced NO production to 19±9% of control (mean±SD, P<0.0001 vs control, n=11), while it did not affect acetylcholine-induced NO production (88±17% of pre-treatment level, P=NS, n=10). In conclusion, hyaluronic acid glycosaminoglycans within the glycocalyx play a pivotal role to detect and amplify the shear force of flowing blood that triggers endothelium-derived NO production in isolated canine femoral arteries.
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