Flow-Induced Arterial Remodeling Relates to Endothelial Function in the Human Forearm

Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Circulation (Impact Factor: 14.43). 07/2008; 117(24):3126-33. DOI: 10.1161/CIRCULATIONAHA.108.778472
Source: PubMed


Chronic changes in blood flow stimulate arterial remodeling, which contributes to the maintenance of vascular homeostasis. Experimental studies suggest that remodeling represents a response to local changes in endothelial shear stress and is nitric oxide-dependent.
To investigate determinants of outward arterial remodeling in humans, we measured ulnar artery flow, diameter, and flow-mediated dilation before and after removal of the adjacent radial artery in 53 patients who were undergoing coronary bypass surgery (age 60+/-11 years; 13% female). Removal of the radial artery increased ulnar artery blood flow by 35% (P=0.009) and increased ulnar artery diameter by 9% (P<0.001) 4 to 8 weeks after surgery. At 1 week, ulnar artery shear stress was increased by 58% (P<0.001), but it was no longer different from baseline at longer-term follow-up. The contralateral ulnar artery was unaffected, which suggests that these findings were not attributable to the systemic effects of medications or the postoperative state. Extent of outward remodeling correlated with the increase in blood flow (r=0.50, P=0.001) and with flow-mediated dilation at baseline (r=0.50, P=0.001). Remodeling correlated inversely with baseline endothelial expression of P-selectin in the radial artery (r=-0.76, P=0.004, n=14).
A sustained increase in blood flow in the ulnar artery induced outward arterial remodeling despite the presence of risk factors and coronary artery disease. The remodeling response was related to endothelial phenotype, as reflected by flow-mediated dilation and expression of P-selectin. These findings provide evidence that the endothelium plays an important role in the regulation of vascular structure in humans.

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    • "Experimental studies have shown that compensatory remodeling depends on the activity of nitric oxide synthase 26, and the authors of these studies recently demonstrated that the remodelling response is blunted in patients with local endothelial dysfunction. Chronic and recurrent limb ischemia stimulates compensatory formation of collateral vessels 27-30, and this response depends on the bioavailabity of nitric oxide 31-33. Thus, endothelial dysfunction may worsen the clinical status in PAD because of impaired formation of collateral vessels and remodelling. "
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