Inhibition of Leucocyte and Platelet Adhesion Reduces Neointimal Hyperplasia after Arterial Injury

Paolo Golino; Giuseppe Ambrosio; Massimo Ragni; Plinio Cirillo; Nicolino Esposito; James T Willerson; Robert Rothlein; Luisa Petrucci; Mario Condorelli; Massimo Chiariello; Maximilian L Buja

doi:10.1055/s-0038-1656050

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1997; 77(04): 783-788
DOI: 10.1055/s-0038-1656050

Animal Models

Schattauer GmbH Stuttgart

Inhibition of Leucocyte and Platelet Adhesion Reduces Neointimal Hyperplasia after Arterial Injury

Authors

Paolo Golino
Giuseppe Ambrosio
Massimo Ragni
Plinio Cirillo
Nicolino Esposito
James T Willerson

²The Department of Immunology, Boehringer-lngelheim Pharmaceuticals, Ridgefield, CT, USA
Robert Rothlein

¹The Department of Internal Medicine, Division of Cardiology 2nd School of Medicine, University of Naples, Italy
Luisa Petrucci
Mario Condorelli
Massimo Chiariello
Maximilian L Buja

³The Departments of Internal Medicine and Pathology, the University of Texas Health Science Center at Houston and the Texas Heart Institute, Houston, TX, USA

Abstract

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Summary

Restenosis following coronary angioplasty is thought to result from migration and proliferation of medial smooth muscle cells. However, the factors that initiate this proliferation are still unknown. In a rabbit model of carotid artery injury, we tested the hypothesis that activated platelets and leucocytes might contribute to the development of neointimal hyperplasia. Following arterial injury, rabbits received either no treatment, R15.7, a monoclonal antibody against the leucocyte CD ll/CD 18 adhesion complex, aurintricarboxylic acid (ATA), a sub stance that inhibits platelet glycoprotein Ib-von Willebrand factor interaction, or the combination of R15.7 and ATA. After 21 days, the extent of neointimal hyperplasia was evaluated by planimetry on histological arterial sections. The area of neointima averaged 0.51 ±0.07 mm² in control animals and it was significantly reduced by administrationof either R15.7 or ATA alone to 0.12 ± 0.05 and 0.20 ±0.01 mm², respectively (p <0.05 vs controls for both groups). The animals that received the combination of R15.7 and ATA showed a further reduction in neointimal hyperplasia, as compared to animals that received ATA alone (p <0.05 vs ATA alone). These data indicate that platelets and leucocytes play animportant role in the pathophysi ology of neointimal hyperplasia in this experimental model. Interven tions that reduce platelet and leucocyte adhesion to vessel wall might have beneficial effects in reducing restenosis following coronary angioplasty.

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References

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