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J Thorac Cardiovasc Surg 1995;110:1005-1012
© 1995 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

REACTIVITY OF HUMAN SAPHENOUS VEINS AT ARTERIAL PERFUSION PRESSURES

Milwaukee, Wis.

Supported by grants NIH HL-29587 (N. J. R.) and HL-41840 (L. E. B.) and an award from the Max Baer Heart Fund of the Fraternal Order of Eagles.

Received for publication Dec. 19, 1994. Accepted for publication March 24, 1995. Address for reprints: Nancy J. Rusch, PhD, Associate Professor of Physiology, Human Vascular Biology Laboratory, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226.

Abstract

Vasospasm of human saphenous vein grafts has been reported after aorta-coronary bypass operations. However, it is unknown whether venoarterial grafts are inherently responsive to vasoconstrictor stimuli after implantation into the arterial circulation or whether their vasomotion is secondary to hemodynamic changes. Thus in this study we used in vitro methods to directly evaluate whether isolated human saphenous vein segments respond to vasoconstrictor agents at arterial pressure levels. External diameter and intraluminal flow were monitored in 12 human saphenous vein segments, which were perfused at 30 ml/min with physiologic salt solution at 90, 70, and 50 mm Hg. Increasing intraluminal pressure higher than 50 mm Hg or exposing the vein to Ca²⁺ -free media did not increase vessel external diameter or intraluminal flow, which suggests that human saphenous veins were fully distended at pressures of 50 mm Hg or greater. However, all human saphenous veins were activated by a 1µmol/L dose of norepinephrine at 50 mm Hg and dilated during subsequent intraluminal infusion of a 1µmol/L dose of acetylcholine, showing intact vascular smooth muscle and endothelial cell function. In the same vessels, a 1µmol/L concentration of 5-hydroxytryptamine constricted human saphenous veins by 19%, 22%, and 26% at intraluminal pressures of 90, 70, and 50 mm Hg, respectively, and reduced vessel flow by 6%, 24%, and 42% at the same pressure levels. Similarly, a 1µmol/L concentration of norepinephrine constricted vessels pressurized at 90, 70, and 50 mm Hg by 9%, 12%, and 17%, respectively, and attenuated vessel flow by as much as 32%. We conclude that human saphenous vein segments are fully distended at perfusion pressures greater than 50 mm Hg, but can dynamically constrict to vasoactive agonists and regulate graft flow at intraluminal pressures as high as 90 mm Hg. Our findings in isolated human saphenous vein segments lend support to clinical observations that human saphenous vein grafts should be regarded as vasoactive conduits after implantation at arterial pressure levels. (J THORAC CARDIOVASC SURG 1995;110:1005-12)

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