Urinary trypsin inhibitor reduced inflammatory response after stent injury in minipig

This study investigated whether urinary trypsin inhibitor (UTI) inhibits neointimal formation by reducing inflammatory response after stent injury. Twenty minipigs having undergone oversized bare material stent implantation in the left anterior descending artery were randomly subdivided into two gro...

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Bibliographic Details
Published in:Pathology, research and practice research and practice, 2012-06, Vol.208 (6), p.344-349
Main Authors: Kong, J.Y., Wang, T.Q., Jiang, G.H., Li, L., Wang, F.P.
Format: Article
Language:English
Subjects:
Animals
Constriction, Pathologic - drug therapy
Constriction, Pathologic - pathology
Coronary Restenosis - drug therapy
Coronary Restenosis - pathology
Coronary Stenosis - pathology
Coronary Vessels - pathology
Coronary Vessels - surgery
Disease Models, Animal
Glycoproteins - pharmacology
Inflammation
Inflammation - drug therapy
Inflammation - pathology
Neointima - chemically induced
Restenosis
Stent
Stents - adverse effects
Swine
Swine, Miniature
Trypsin Inhibitors - pharmacology
Urinary trypsin inhibitor
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Summary:This study investigated whether urinary trypsin inhibitor (UTI) inhibits neointimal formation by reducing inflammatory response after stent injury. Twenty minipigs having undergone oversized bare material stent implantation in the left anterior descending artery were randomly subdivided into two groups: a UTI group (n=10) and a control group (n=10). Two systemic markers of inflammation (serum macrophage chemoattractant protein-1 and interleukin-6 levels measured by ELISA) were increased after stent implantation, and two days after stem implantation, their levels were positively correlated with the maximal percentage of area stenosis on day 28 (r2=0.889 and 0.743, respectively). This effect was abolished by UTI administration. Twenty-eight days after implantation, morphometric analysis of the stented arteries revealed significantly reduced luminal stenosis (38±6% vs. 64±12%, P
ISSN:0344-0338
1618-0631
DOI:10.1016/j.prp.2012.03.008