MECHANISMS OF VEIN GRAFT ATHEROSCLEROSIS - LDL METABOLISM AND ENDOTHELIAL ACTIN REORGANIZATION

被引:36
作者
BERCELI, SA
BOROVETZ, HS
SHEPPECK, RA
MOOSA, HH
WARTY, VS
ARMANY, MA
HERMAN, IM
机构
[1] UNIV PITTSBURGH, SCH MED, DEPT SURG, PITTSBURGH, PA 15261 USA
[2] LIFENET, PITTSBURGH TISSUE BANK, VIRGINIA BEACH, VA USA
[3] UNIV PITTSBURGH, SCH MED, DEPT PATHOL, PITTSBURGH, PA 15261 USA
[4] TUFTS UNIV, SCH HLTH SCI, PROGRAM CELL MOLEC & DEV BIOL, BOSTON, MA 02111 USA
关键词
D O I
10.1016/0741-5214(91)90227-L
中图分类号
R61 [外科手术学];
学科分类号
摘要
We have explored the effect of arterial hemodynamics on endothelial cell morphology and low-density lipoprotein metabolism in human saphenous vein segments harvested from tissue donors. An arterial pulsatile perfusion system was used to impose physiologic pressures and flows for 20 hours on saphenous vein and companion (control) femoral artery segments. A venous perfusion apparatus was also employed for the perfusion of a second (control) saphenous vein segment for the same period of time. Calculations of fluid shearing and wall tensile stresses were performed and related to induced changes in endothelial cell geometry and cytoskeletal actin organization and the incorporation, degradation, and localization of intact low-density lipoprotein within the vessel wall. Our results indicate that, compared with native arteries and veins, a 20-hour exposure of test saphenous veins to arterial hemodynamics induced (1) a significant increase in endothelial cell luminal surface area and perimeter independent of alignment with flow, (2) disassembly of the dense peripheral band of actin with a concomitant assembly of stress fibers, and (3) a two- to fourfold elevation in the undergraded low-density lipoprotein content, localized primarily within the subendothelial intima. Although the exact mechanisms underlying these results are uncertain, the focal accumulation of intramural low-density lipoprotein may be related to the loss of normal barrier function during endothelial cell enlargement, which is accompanied by transient cytoskeletal reorganization during the adaptation to arterial flow.
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页码:336 / 347
页数:12
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