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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An "optimal" technique of vein graft preparation with papaverine and tissue culture was compared with an "injury" technique with 37 degrees C saline storage for 1 hr. Paired interposition cephalic vein grafts were placed in the femoral arteries of dogs. Specimens were taken at the time of implantation, at 3 and 24 hr, and at 7 and 30 days for light, scanning, and transmission electron microscopy. Veins obtained by the injury method showed extensive initial disruption of the endothelium and platelet and white cell adhesion at 3 and 24 hr. At 7 days the endothelium was restored, but there was marked inflammation and neovascularization of the media. At 30 days this had resolved; however, the smooth muscle cells appeared modulated (increase in relative numbers of metabolic organelles with contractile apparatus disassembly). Extracellular matrix was substantially increased, with abundant amorphous ground substance. In contrast, veins obtained by the optimal method had intact endothelium both at implantation and thereafter. Adhesion of white cells and platelets to the endothelium did not occur. The media remained compact without inflammation and without modulation of the smooth muscle cells. We conclude that vein grafts prepared by the optimal technique do not develop early or late evidence of endothelial or medial injury. This should result in a nonthrombogenic graft immediately after surgery and diminished late intimal/medial hyperplasia.
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PMID:Integrity of vein grafts as a function of initial intimal and medial preservation. 687 81

Microvascular complications in sickle cell disease occur as a result of obstruction of small vessels by deoxygenated sickle cells. Cerebrovascular complications are also common and result from obstruction of large blood vessels by thrombosis with changes in vessels that have some similarity to those found in arteriosclerotic vascular disease. Endothelial damage and activation from sickle cell-endothelial interactions may contribute to both. We find that endothelial cells have increased expression of VCAM-1, E-selectin, and ICAM-1 when exposed to sickle blood cells. The concentration-dependent, sickle-induced, adhesion molecule expression is significantly greater than that promoted by normal cells. The time course of Cell Adhesion Molecule (CAM) expression is similar to that induced by TNF-alpha and IL1. Studies after white cell enrichment and reduction suggest leukocytes are the primary mediators. CAM expression by endothelial cells appears stimulated by soluble factors. Antibody inhibition studies support TNF-alpha and IL-1, produced by sickle leukocytes, as the primary soluble factors responsible for the observed CAM expression. Both the induction of endothelial CAM expression and subsequent endothelial adherence of sickle erythrocytes may play significant roles in the pathophysiology of sickle-related complications, and reduction in CAM expression may provide a new approach to treatment.
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PMID:Activation of vascular endothelial cell adhesion molecule expression by sickle blood cells. 1267 44