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Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Reactive oxygen species cause endothelial dysfunction in chronic flow overload.

X Lu¹, X Guo, C D Wassall

¹Department of Biomedical Engineering, Indiana Univ. Purdue Univ. Indianapolis, Indianapolis, IN 46202, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)

|December 4, 2010

Summary

Chronic flow overload increases vascular reactive oxygen species (ROS) production via NADPH oxidase, leading to endothelial dysfunction. Antioxidant treatment mitigated these effects, suggesting ROS involvement in flow-induced vascular changes.

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Area of Science:

Cardiovascular Physiology
Vascular Biology
Oxidative Stress Research

Background:

Elevated shear stress is known to increase vascular reactive oxygen species (ROS) production.
The specific role of ROS in chronic flow overload (CFO) and subsequent endothelial dysfunction remains under-investigated.

Purpose of the Study:

To investigate the hypothesis that CFO increases ROS production, partly mediated by NADPH oxidase, leading to endothelial dysfunction.
To examine the effects of apocynin, an NADPH oxidase inhibitor, on ROS production and endothelial function in a swine model of CFO.

Main Methods:

Chronic flow overload (CFO) was induced in swine carotid arteries via contralateral ligation for one week.
Apocynin treatment was administered to a subset of swine undergoing CFO.
Measurements included blood flow, arterial diameter, gene/protein expression (eNOS, p22/p47phox, NOX2/NOX4), ROS production, and endothelium-dependent vasorelaxation.

Main Results:

CFO significantly increased carotid artery blood flow and diameter, alongside upregulated expressions of eNOS, p22/p47phox, and NOX2/NOX4.
ROS production increased threefold in CFO swine, correlating with compromised endothelium-dependent vasorelaxation.
Apocynin treatment reduced ROS production, preserved endothelial function, and inhibited the expression of key NADPH oxidase components.

Conclusions:

CFO induces endothelial dysfunction within one week, characterized by increased ROS production mediated by NADPH oxidase.
Apocynin treatment effectively counteracts CFO-induced ROS production and endothelial dysfunction.
These findings implicate NADPH oxidase-derived ROS and endothelial nitric oxide synthase (eNOS) uncoupling in the early stages of CFO-induced vascular remodeling.