ヒト冠状動脈における傷害後の細胞組織反応

• 上田 真喜子

  Department of Pathology, Osaka City University Medical School

• 笠行 典章

  Department of Pathology, Osaka City University Medical School

• 章 立新

  Department of Pathology, Osaka City University Medical School

• 成子 隆彦

  First Department of Internal Medicine, Osaka City University Medical School

• 大谷 眞一郎

  First Department of Internal Medicine, Osaka City University Medical School

• 高木 雅彦

  First Department of Internal Medicine, Osaka City University Medical School

書誌事項

タイトル別名

• Cellular Reactions at the Angioplasty Injury Site in Human Coronary Arteries

抄録

Percutaneous transluminal coronary angioplasty (PTCA) has become widely accepted as the preferred treatment for selected patients with acutely or chronically obstructed coronary arteries. Pathological observations of human coronary arteries after PTCA have suggested that arterial-wall and plaque injuries are the primary mechanisms of dilation in PTCA. The present study focused on cellular reactions at the angioplasty injury site in autopsied patients who had died after being subjected to PTCA.<br>Seventy-one hearts including 106 PTCA sites were available for this study. The interval between PTCA and death at these sites varied from three hours to three years and three months. The localization of the angioplasty site was determined by correlation between the specimens and the angiograms taken when the procedure was carried out. The coronary arteries subjected to the angioplasty were sectioned serially at 1-mm intervals and examined. To conduct immunocytochemical investigations, the following monoclonal antibodies were used: antimuscle actin antibody, HHF 35; anti-smooth muscle actin antibody, CGA 7 ; anti-vimentin antibody; anti-desmin antibody; anti-macrophage antibody, HAM 56; anti-factor VIII-related antigen antibody.<br>All the dilated sites revealed an angioplasty injury of the coronary arterial wall. In cases of a medial angioplasty injury, the earliest cellular response was observed 5 days after PTCA, and was characterized by de-differentiation of the medial smooth muscle cells and the appearance of spindle-shaped cells at the injury site. At the earliest stage, the cells in the reactive tissue failed to express smooth muscle cell actin. However, during evolution of the reactive tissue, re-differentiation of smooth muscle cells occurred, as revealed by changes in the actin expression. Injury to an atheroma caused a different type of cellular response. At these sites, plaque hemorrhage often dominated the lesion, resulting in a proliferation of organization tissue. Immunocytochemical staining showed that the repair tissue at the atheroma injury site was composed of macrophages, smooth muscle cells and small vessels.<br>These findings indicate that in the cellular response that followed angioplasty injury of a human coronary artery: 1) spindle-shaped cells within the reactive tissue at the earliest stage reveal cytoskeletal features consistent with a de-differentiated smooth muscle cell phenotype; 2) during evolution of the reactive tissue, smooth muscle cells revert to cytoskeletal features reflecting re-differentiation.

収録刊行物

• 動脈硬化

  動脈硬化 21 (6), 479-485, 1993

  一般社団法人 日本動脈硬化学会

詳細情報

• CRID: 1571135652960741504
• NII論文ID: 130006849324
• データソース種別:
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