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Increased Vascular Injury Reduces the Degree of Intimal Hyperplasia following Angioplasty in Rabbits.

Journal article
Authors Per Fogelstrand
Stefan Mellander
Erney Mattsson
Published in Journal of vascular research
Volume 48
Issue 4
Pages 307-15
ISSN 1423-0135
Publication year 2011
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Institute of Clinical Sciences
Pages 307-15
Language en
Keywords restenos, adventitia, intimal hyperplasi, glatta muskelceller
Subject categories Medical and Health Sciences, Cell and Molecular Biology, Surgery


Background/Aims: Formation of intimal hyperplasia following angioplastic procedures can lead to complications, including restenosis and accelerated atherosclerosis. The vessel wall media is a main source of neointimal cells. However, evidence suggests that there are additional cell sources, such as the adventitia. Here we investigate whether an extensive loss of vascular smooth muscle cells (VSMCs) in the media results in less intimal hyperplasia or if there is compensatory cell recruitment from the adventitia. Methods:A balloon catheter was pulled through the rabbit carotid artery 4 times (major injury) or 2 times (minor injury). Adventitial cells were labeled with 5-bromo-2-deoxyuridine or PKH26. Results:The major injury, but not the minor injury, resulted in a complete loss of VSMCs in large parts of the media and significant leukocyte infiltration. The major injury resulted in less neointima compared with the minor injury. The thinnest neointima was seen at the most injured parts of the media in the major injury group. Cell-tracking experiments showed that the media, but not the adventitia, served as a source of neointimal cells. Conclusion: An augmented angioplastic injury with extensive VSMC loss in rabbits reduced the degree of intimal hyperplasia. No compensatory recruitment of neointimal cells from the adventitia occurred.

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