外膜
医学
病理
炎症
川地68
动脉瘤
主动脉瘤
主动脉夹层
主动脉
免疫组织化学
免疫学
心脏病学
外科
作者
Danli Wu,Justin Chin-Bong Choi,Aryan Sameri,Charles G. Minard,Joseph S. Coselli,Ying H. Shen,Scott A. LeMaire
出处
期刊:Aorta
[Georg Thieme Verlag KG]
日期:2013-12-01
卷期号:1 (6): 259-267
被引量:35
标识
DOI:10.12945/j.aorta.2013.13-044
摘要
Thoracic aortic dissection (TAD) is a highly lethal cardiovascular disease. Injury to the intima and media allows pulsatile blood to enter the media, leading to dissection formation. Inflammatory cells then infiltrate the site of aortic injury to clear dead cells and damaged tissue. This excessive inflammation may play a role in aneurysm formation after dissection.Using immunohistochemistry, we compared aortic tissues from patients with acute TAD (n = 11), patients with chronic TAD (n = 35), and donor controls (n = 20) for the presence of CD68+ macrophages, neutrophils, mast cells, and CD3+ T lymphocytes.Tissue samples from patients with acute or chronic TAD generally had significantly more inflammatory cells in both the medial and adventitial layers than did the control samples. In tissues from patients with acute TAD, the adventitia had more of the inflammatory cells studied than did the media. The pattern of increase in inflammatory cells was similar in chronic and acute TAD tissues, except for macrophages, which were seen more frequently in the adventitial layer of acute TAD tissue than in the adventitia of chronic TAD tissue.The inflammatory cell content of both acute and chronic TAD tissue was significantly different from that of control tissue. However, the inflammatory cell profile of aneurysmal chronic TAD was similar to that of acute TAD. This may reflect a sustained injury response that contributes to medial degeneration and aneurysm formation.
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