Effect of increased intraluminal pressure on human saphenous vein vasomotor function in vitro


Journal Article

When used as bypass conduits, human saphenous veins are exposed to systemic arterial pressure. Owing to the relative thickness of the smooth muscle cell layer of the saphenous vein, however, it must often be exposed to supraphysiologic pressure to fully distend and overcome spasm. This study examined the effect of exposure of human saphenous veins to physiologic and supraphysiologic intraluminal pressure on smooth muscle and endothelial cell function. Ten portions of saphenous vein were obtained from patients undergoing peripheral or aortorenal bypass procedures. Adjacent segments were mounted in a perfusion chamber and statically inflated with Krebs solution for 10 minutes at 150 mm Hg pressure (n = 5) or 300 mm Hg pressure (n = 5). Adjacent segments were filled with Krebs solution under no pressure (n = 10). Vein rings (1-2 rings per segment) were then tested in an organ bath for isometric contraction in response to potassium chloride 60 mM, norepinephrine 10-9 M to 10-4 M, and histamine 10-8 M to 10-4 M, as well as relaxation following norepinephrine precontraction in response to acetylcholine 10-8 M to 10-4 M, sodium nitroprusside 10-8 M to 10-4 M, and calcium ionophore A23187 10-8 M to 10-4 M. Vein segments distended at 150 mm Hg contracted less than their control counterparts, although the differences did not reach statistical significance. Distension of vein segments at 300 mm Hg, however, led to a significant decline in contractions in response to KCl (1.50 ± 0.42 g; p < .05 compared with control) and norepinephrine (2.61 ± 0.68 g; p < .05), as well as a further decline in contractions in response to histamine that failed to reach statistical significance (2.19 ± 0.69 g). There were no differences with respect to catecholamine sensitivity (LD50 value), endothelium-dependent relaxation, or endothelium-independent relaxation. We conclude that the human saphenous vein can retain much of its contractile function when exposed to arterial pressures. At supraphysiologic pressure (i.e., 300 mm Hg), however, contractile function is attenuated to approximately 20% of control levels. These data support the clinical observation that pressurization of veins during preparation for bypass must often exceed arterial pressure to overcome smooth muscle spasm.

Duke Authors

Cited Authors

  • Schwartz, LB; Massey, MG; Hagen, PO; McCann, RL

Published Date

  • January 1, 1994

Published In

  • Journal of Vascular Medicine and Biology

Volume / Issue

  • 5 / 1-2

Start / End Page

  • 31 - 37

International Standard Serial Number (ISSN)

  • 1042-5268

Citation Source

  • Scopus