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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

Paolo Golino
,
Giuseppe Ambrosio
,
Massimo Ragni
,
Plinio Cirillo
,
Nicolino Esposito
,
James T Willerson
2   The Department of Immunology, Boehringer-lngelheim Pharmaceuticals, Ridgefield, CT, USA
,
Robert Rothlein
1   The Department of Internal Medicine, Division of Cardiology 2nd School of Medicine, University of Naples, Italy
,
Luisa Petrucci
,
Mario Condorelli
,
Massimo Chiariello
,
Maximilian L Buja
3   The Departments of Internal Medicine and Pathology, the University of Texas Health Science Center at Houston and the Texas Heart Institute, Houston, TX, USA
› Author Affiliations
Further Information

Publication History

Received 25 July 1996

Accepted after revision 27 October 1996

Publication Date:
11 July 2018 (online)

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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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