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KMID : 0350519950480030767
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Journal of Catholic Medical College
1995 Volume.48 No. 3 p.767 ~ p.775
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The Inhibitory Effects of Heparin and Cyclosporin A on the Intimal Hyperplasia after Arterial Injury in Rat
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Abstract
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Intimal hyperplasia, smooth muscle cell migration and proliferation with the formation of extracellular matrix, may occur after arterial injury and is a frequent causes of failure after endarterectomy, autologous vein grafting, and balloon
catheter
embolectomy. The precise pathophysiologic pathways leading to the development of intimal hyperplasia have not been characterized. Recent data suggested that damaged smooth muscle cells (SMCs) might be releasing some kind of intracellular factor
that
would then stimulate the remaining SMCs. A logical candidate is the basic fibroblast growth factor (bFGF) since it can be released from disrupted cultured vascular cells.
Immunologic mechanisms may also be important in the response of the vessel to injury. Mononuclear cells have been shown to adhere to sites of arterial injury by balloon catheter denudation of rabbit aortas and remain in the vascular proliferative
lesions at those areas for up to 6 weeks. The stimulus for their presence in this lesion is unclear, but mononuclear cells are known to respond to a variety of lymphokines. Additional evidence showing that immunologic mechanisms may play a role
in
the
development of vascular proliferative or atherosclerotic lesions is based on the work that activated SMCs associated with experimental arterial injury express classⅡantigens of the major histocompatibility comlex (MHC), whereas normal arteries
express
none of T lymphocytes.
This study was undertaken to examine the effect of cyclosporin A (CsA) on the development of proliferative intimal lesion after experimental arterial injury in a rat model.
Aortic denudation was performed by balloon catheter. The rats were divided into three groups : Control group, normal feeding ; CsA GROUP, CsA 3 mg/kg/day subcutaneously ; heparin group, heparin 1200 U/kg/day subcutaneously The animals were
sacrified and
aortas were perfused and fixed T at 21 days after denudation. Microscopic findings were observed and cross-sectional intima-to-media (I-M ratio) were calculated by image analyzer system.
@ES The results were as follows :
@EN 1. Microscopic findings of the control group show severe intimal hyperplasia, Intimal hyperplasia of the heparin group and the CsA group reduce more significantly than the control group The intimal hyperplsia in reponse to injury is the
result
of
the new accumulation of proliferating SMC and connective tissue.
2. Intima was markedly thickened and mean I-M ratio of 107.1±14.3% in the control group. In contrast the I-m ratio in the heparin group was reduced to 47.9±5.15% (P<0.05), CsA group 46.9±10.63 (P<0.05).
In conclusion, our data showed that heparin and CaA effectively inhibits the development of an intimal thickening during the arterial response to injury. Furthermore, this study has provided additional evidence to support the concept of an
immunologic
mechanism that may play an important role in the development of vascular proliferative lesions.
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KEYWORD
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