Arterial Adaptation to Increased Wall Shear Stress

Abstract

The timing and magnitude of arterial dilation in response to increased flow velocities and the effect on wall shear stress were evaluated in a chronic nonatherogenic animal model. A 7 mm femoral arteriovenous fistula was constructed in one groin in 10 mongrel dogs, the other groin serving as a control. Duplex ultrasound was used at regular intervals to make bilateral measurements of systolic and diastolic luminal diameters, peak systolic velocity, and volume flows to allow estimation of wall shear stress and any vasodilation; measured systemic pulse pressure was used to calculate compliance. Data were acquired at baseline; immediately postoperatively; at one and two weeks, and at one, three, five, and seven months. There were no significant changes from baseline in control vessels at any time interval in blood flow (135 ±56 mL/min), lumen diameter (4.4 ±0.4 mm), wall shear stress (8.8 ±4.3 dynes/cm²), or compliance (0.14 ±0.04 %/mmHg). In the experimental vessels, baseline values were not significantly different from those seen on the control side. Immediate postoperative fistula flow was 1590 ±295 mL/minute, and these flow values were maintained throughout the study. Immediately postoperatively the luminal diameter increased to 5.6 ±0.5 mm with a calculated shear stress of 49.8 ±14.1 dynes/cm ² (P < 0.001 compared with baseline). This increase in luminal diameter and the resulting shear stress remained essentially constant throughout the study, with values of 5.8 ±0.3 mm and 47.0 ± 11.5 dynes/cm², respectively, at seven months. No significant changes in compliance were seen during the study. The authors conclude that increased blood flow alone causes early moderate arterial dilation but will not produce a complete normalization of wall shear stress. For that to occur, additional mechanisms may be involved relating increased shear stress and dysfunctional vascular endothelium, such as occurs in hypercholesterolemia.