Publication: Inflammatory cells induce neointimal growth in a rat arterial autograft model
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Date
2002
Authors
Jurado, F. ; Bellón, J.M. ; Rodríguez, M. ; Corrales, C. ; Buján, J.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Subendothelial invasion by leukocytes is a
sign of intimal thickening in arteriosclerosis and in the
response of a vessel to mechanical damage. Our study
was designed to establish whether these cells are
implicated in the formation of a neointima in an
autologous arterial graft model in the rat and to evaluate
the effects of cyclosporin A (CsA). Three study groups
were established according to whether the animals were
treated with CsA-Cp (Sandimmun)®, CsA-Et (ethanol
vehicle) or received no treatment (control group). Both
drug forms were administered (5 mg/kg/day, s.c.) from 4
days prior to surgery until the time of sacrifice.
Antibodies specific for lymphocytes (CD4, CD8),
monocytes/macrophages-ED1, smooth muscle a-actin
and the von Willebrand factor (vWF) were used to
identify the cells in the grafted arterial wall. In control
grafts, the neointima had formed by 2 weeks postimplant.
However, the cells comprising this layer
generally presented no positivity whatsoever towards the
antibodies employed. At 50 days, the new layer was
observed to be formed by a vWF-positive endothelium
and a-actin-positive cells. In all three groups, several
polymorphonuclear (PMN) cells adhered to the denuded
luminal surface from 7 days onwards. In the treated
animals, neutrophils and monocytes were seen to
infiltrate intimal and medial layers during the later postimplant
stages. Around the third week post-implant, the
neointima had reached the grafted segment from the
distal portion of the recipient artery, and by 50 days it
was similar to that seen in control specimens. Our
findings suggest that: a) neutrophils play a role in
neointimal thickening in this arterial autograft model;
and b) CsA promotes the adhesion and infiltration of
neutrophils in the injured arterial wall.
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