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  • Title: Morphometric and immunocytochemical analysis of coronary arterioles in human transplanted hearts.
    Author: Armstrong AT, Strauch AR, Kardan A, Starling RC.
    Journal: J Heart Lung Transplant; 1996 Aug; 15(8):818-26. PubMed ID: 8878764.
    Abstract:
    BACKGROUND: Heart transplant vascular sclerosis has been characterized in epicardial coronaries of human transplanted hearts. The purpose of this study was to analyze coronary arterioles (< 100 microns in diameter) within endomyocardial biopsy specimens from heart transplant recipients for the presence of disease. METHODS: The morphologic compartments of trichrome-stained vessels were quantified by means of computer imaging to measure the percentage of stenosis of 164 arterioles from 30 transplant recipients over time. The arterioles were divided into three groups based on their biopsy date after transplantation: early (0 to 6 months), middle (6 to 18 months), and late (18 to 36 months). The percentage of stenosis of arterioles from a control group of nondiseased hearts was compared with the grafts. Also, arterioles from heart transplant recipients were immunohistochemically labeled with an antibody, PC10, specific for proliferating cell nuclear antigen. The arterioles were immunocytochemically labeled with an antibody specific for vascular smooth muscle alpha-actin and the fluorescent signal was analyzed. RESULTS: The percentage of stenosis was not significantly different among the early, middle, late, and control groups. Vessels from the early, middle, and late groups did not show binding of the PCNA antibody. The antibody signal intensity and amount of alpha-actin within each vessel was significantly higher in the late groups as compared with the early and middle groups. CONCLUSIONS: The coronary microvasculature of human transplanted hearts does not exhibit intimal thickening or cellular proliferation within 3 years after transplantation. However, as shown by an increase of smooth muscle alpha-actin over time, vascular remodeling may occur in response to cytokines released as a result of injury.
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