In vivo human lower extremity saphenous vein bypass grafts manifest flow mediated vasodilation

Christopher D. Owens, Nicole Wake, Michael S. Conte, Marie Gerhard-Herman, Joshua A. Beckman

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Objective: As in arteries, venous endothelium modulates vessel homeostasis and tone. The effect of an arterialized environment on venous endothelial function remains poorly understood. In particular, regulation of saphenous vein graft (SVG) blood flow and lumen caliber remains undefined. We hypothesized that mature SVGs would exhibit endothelium-dependent, flow-mediated vasodilation (FMD). We further hypothesized that endothelium-derived nitric oxide (NO) was an important mediator. Methods: Patients with femoral to popliteal artery SVGs that had maintained primary patency and were at least 1 year from surgery were enrolled. High-resolution, B-mode ultrasound scans were used to measure vein graft diameter before and 1 minute after reactive hyperemia (RH) to determine FMD. RH was created through application of 220 mm Hg to the calf for 5 minutes with a sphygmomanometric cuff. After a 10-minute recovery period, nitroglycerin-mediated, endothelium-independent vasodilation was measured 3 minutes after administration of nitroglycerin 0.4 mg sublingually. Brachial artery FMD was determined by validated techniques. L-NGmonomethyl arginine (L-NMMA; 1 mg/kg infusion over 10 minutes) was used in a subset of patients (n = 6) to competitively inhibit endothelial NO synthase. Results: Nineteen subjects were enrolled. The median age of the SVGs was 34.6 (21.0-49.7) months. SVG flow-mediated, endothelium-dependent vasodilation was measured at 5.28% ± 3.1% mean change in lumen diameter (range, 1.99%-9.36%; P < .0001 for diameter change). Nitroglycerin-mediated vasodilation was 3.7% ± 1.0%, (range, 16%-10.04%; P < .005). Intravenous administration of L-NMMA abolished SVG FMD (5.7 ± 1.4% before L-NMMA vs 0.01 ± 0.01% during L-NMMA infusion; P = .0088) and attenuated brachial artery FMD (7.54% ± 1.0% vs 5.7 ± 1.4; P = .05). Conclusion: SVGs manifest flow-mediated, endothelium-dependent, and nitroglycerin-mediated endothelium-independent vasodilation. Vein graft endothelium-dependent FMD is likely mediated by NO. Further investigation will be required to determine the role of endothelial function in vein graft patency.

Original languageEnglish (US)
Pages (from-to)1063-1070
Number of pages8
JournalJournal of Vascular Surgery
Volume50
Issue number5
DOIs
StatePublished - Nov 1 2009
Externally publishedYes

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Saphenous Vein
Vasodilation
Lower Extremity
Transplants
Endothelium
omega-N-Methylarginine
Nitroglycerin
Veins
Brachial Artery
Hyperemia
Nitric Oxide
Popliteal Artery
Nitric Oxide Synthase Type III
Thigh
Intravenous Administration
Arginine
Homeostasis
Arteries

ASJC Scopus subject areas

  • Surgery
  • Cardiology and Cardiovascular Medicine

Cite this

In vivo human lower extremity saphenous vein bypass grafts manifest flow mediated vasodilation. / Owens, Christopher D.; Wake, Nicole; Conte, Michael S.; Gerhard-Herman, Marie; Beckman, Joshua A.

In: Journal of Vascular Surgery, Vol. 50, No. 5, 01.11.2009, p. 1063-1070.

Research output: Contribution to journalArticle

Owens, Christopher D. ; Wake, Nicole ; Conte, Michael S. ; Gerhard-Herman, Marie ; Beckman, Joshua A. / In vivo human lower extremity saphenous vein bypass grafts manifest flow mediated vasodilation. In: Journal of Vascular Surgery. 2009 ; Vol. 50, No. 5. pp. 1063-1070.
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abstract = "Objective: As in arteries, venous endothelium modulates vessel homeostasis and tone. The effect of an arterialized environment on venous endothelial function remains poorly understood. In particular, regulation of saphenous vein graft (SVG) blood flow and lumen caliber remains undefined. We hypothesized that mature SVGs would exhibit endothelium-dependent, flow-mediated vasodilation (FMD). We further hypothesized that endothelium-derived nitric oxide (NO) was an important mediator. Methods: Patients with femoral to popliteal artery SVGs that had maintained primary patency and were at least 1 year from surgery were enrolled. High-resolution, B-mode ultrasound scans were used to measure vein graft diameter before and 1 minute after reactive hyperemia (RH) to determine FMD. RH was created through application of 220 mm Hg to the calf for 5 minutes with a sphygmomanometric cuff. After a 10-minute recovery period, nitroglycerin-mediated, endothelium-independent vasodilation was measured 3 minutes after administration of nitroglycerin 0.4 mg sublingually. Brachial artery FMD was determined by validated techniques. L-NGmonomethyl arginine (L-NMMA; 1 mg/kg infusion over 10 minutes) was used in a subset of patients (n = 6) to competitively inhibit endothelial NO synthase. Results: Nineteen subjects were enrolled. The median age of the SVGs was 34.6 (21.0-49.7) months. SVG flow-mediated, endothelium-dependent vasodilation was measured at 5.28{\%} ± 3.1{\%} mean change in lumen diameter (range, 1.99{\%}-9.36{\%}; P < .0001 for diameter change). Nitroglycerin-mediated vasodilation was 3.7{\%} ± 1.0{\%}, (range, 16{\%}-10.04{\%}; P < .005). Intravenous administration of L-NMMA abolished SVG FMD (5.7 ± 1.4{\%} before L-NMMA vs 0.01 ± 0.01{\%} during L-NMMA infusion; P = .0088) and attenuated brachial artery FMD (7.54{\%} ± 1.0{\%} vs 5.7 ± 1.4; P = .05). Conclusion: SVGs manifest flow-mediated, endothelium-dependent, and nitroglycerin-mediated endothelium-independent vasodilation. Vein graft endothelium-dependent FMD is likely mediated by NO. Further investigation will be required to determine the role of endothelial function in vein graft patency.",
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T1 - In vivo human lower extremity saphenous vein bypass grafts manifest flow mediated vasodilation

AU - Owens, Christopher D.

AU - Wake, Nicole

AU - Conte, Michael S.

AU - Gerhard-Herman, Marie

AU - Beckman, Joshua A.

PY - 2009/11/1

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N2 - Objective: As in arteries, venous endothelium modulates vessel homeostasis and tone. The effect of an arterialized environment on venous endothelial function remains poorly understood. In particular, regulation of saphenous vein graft (SVG) blood flow and lumen caliber remains undefined. We hypothesized that mature SVGs would exhibit endothelium-dependent, flow-mediated vasodilation (FMD). We further hypothesized that endothelium-derived nitric oxide (NO) was an important mediator. Methods: Patients with femoral to popliteal artery SVGs that had maintained primary patency and were at least 1 year from surgery were enrolled. High-resolution, B-mode ultrasound scans were used to measure vein graft diameter before and 1 minute after reactive hyperemia (RH) to determine FMD. RH was created through application of 220 mm Hg to the calf for 5 minutes with a sphygmomanometric cuff. After a 10-minute recovery period, nitroglycerin-mediated, endothelium-independent vasodilation was measured 3 minutes after administration of nitroglycerin 0.4 mg sublingually. Brachial artery FMD was determined by validated techniques. L-NGmonomethyl arginine (L-NMMA; 1 mg/kg infusion over 10 minutes) was used in a subset of patients (n = 6) to competitively inhibit endothelial NO synthase. Results: Nineteen subjects were enrolled. The median age of the SVGs was 34.6 (21.0-49.7) months. SVG flow-mediated, endothelium-dependent vasodilation was measured at 5.28% ± 3.1% mean change in lumen diameter (range, 1.99%-9.36%; P < .0001 for diameter change). Nitroglycerin-mediated vasodilation was 3.7% ± 1.0%, (range, 16%-10.04%; P < .005). Intravenous administration of L-NMMA abolished SVG FMD (5.7 ± 1.4% before L-NMMA vs 0.01 ± 0.01% during L-NMMA infusion; P = .0088) and attenuated brachial artery FMD (7.54% ± 1.0% vs 5.7 ± 1.4; P = .05). Conclusion: SVGs manifest flow-mediated, endothelium-dependent, and nitroglycerin-mediated endothelium-independent vasodilation. Vein graft endothelium-dependent FMD is likely mediated by NO. Further investigation will be required to determine the role of endothelial function in vein graft patency.

AB - Objective: As in arteries, venous endothelium modulates vessel homeostasis and tone. The effect of an arterialized environment on venous endothelial function remains poorly understood. In particular, regulation of saphenous vein graft (SVG) blood flow and lumen caliber remains undefined. We hypothesized that mature SVGs would exhibit endothelium-dependent, flow-mediated vasodilation (FMD). We further hypothesized that endothelium-derived nitric oxide (NO) was an important mediator. Methods: Patients with femoral to popliteal artery SVGs that had maintained primary patency and were at least 1 year from surgery were enrolled. High-resolution, B-mode ultrasound scans were used to measure vein graft diameter before and 1 minute after reactive hyperemia (RH) to determine FMD. RH was created through application of 220 mm Hg to the calf for 5 minutes with a sphygmomanometric cuff. After a 10-minute recovery period, nitroglycerin-mediated, endothelium-independent vasodilation was measured 3 minutes after administration of nitroglycerin 0.4 mg sublingually. Brachial artery FMD was determined by validated techniques. L-NGmonomethyl arginine (L-NMMA; 1 mg/kg infusion over 10 minutes) was used in a subset of patients (n = 6) to competitively inhibit endothelial NO synthase. Results: Nineteen subjects were enrolled. The median age of the SVGs was 34.6 (21.0-49.7) months. SVG flow-mediated, endothelium-dependent vasodilation was measured at 5.28% ± 3.1% mean change in lumen diameter (range, 1.99%-9.36%; P < .0001 for diameter change). Nitroglycerin-mediated vasodilation was 3.7% ± 1.0%, (range, 16%-10.04%; P < .005). Intravenous administration of L-NMMA abolished SVG FMD (5.7 ± 1.4% before L-NMMA vs 0.01 ± 0.01% during L-NMMA infusion; P = .0088) and attenuated brachial artery FMD (7.54% ± 1.0% vs 5.7 ± 1.4; P = .05). Conclusion: SVGs manifest flow-mediated, endothelium-dependent, and nitroglycerin-mediated endothelium-independent vasodilation. Vein graft endothelium-dependent FMD is likely mediated by NO. Further investigation will be required to determine the role of endothelial function in vein graft patency.

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