Robert S Poston, Margaret E Billingham, Jeffrey Pollard, E

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Date of download: 6/3/2016 Copyright © The American College of Cardiology. All rights reserved. From: SOCS1 Prevents Graft Arteriosclerosis by Preserving.

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Effects of Increased ICAM-1 on Reperfusion Injury and Chronic Graft Vascular Disease Robert S Poston, Margaret E Billingham, Jeffrey Pollard, E.Grant Hoyt, Robert C Robbins The Annals of Thoracic Surgery Volume 64, Issue 4, Pages 1004-1012 (October 1997) DOI: 10.1016/S0003-4975(97)00816-3

Fig. 1 Northern blot analysis of intercellular adhesion molecule-1 (ICAM-1) mRNA expression in reperfused allografts. (A) Hearts harvested from healthy donors failed to reveal the 2.8-kb ICAM-1 messenger RNA band (as shown in the positive control lane) at any of the postoperative time points. (B) Hearts harvested from lipopolysaccharide (LPS)-pretreated rats demonstrated weak ICAM-1 bands after 12 and 24 hours of reperfusion as shown by 2.8-kb bands from the grafts that are darker than those from the native ACI heart, which serves as the internal negative control. (° = hours.) The Annals of Thoracic Surgery 1997 64, 1004-1012DOI: (10.1016/S0003-4975(97)00816-3)

Fig. 2 Immunohistochemical analysis of intercellular adhesion molecule-1 (ICAM-1) protein expression in reperfused allografts. (Top left) Hearts harvested from healthy donors displayed only weak ICAM-1 staining on the endothelium of capillaries and veins (thin arrow) that was absent on arteries (large arrow) at baseline before reperfusion (original magnification, ×100). This pattern did not change after 6 or 12 hours of reperfusion; however, (top right) after 24 hours, weak ICAM-1 staining was noted on the intercalated disks of myocytes (arrowheads) (original magnification, ×50). (Bottom left) Hearts from lipopolysaccharide (LPS)-pretreated (Rx’ed) donors displayed stronger ICAM-1 staining on the endothelium of capillaries, veins (thin arrow), and also arteries (large arrow), but not myocytes before transplantation (×100). (Bottom right) After reperfusion for 24 hours, a dramatic increase in the expression of ICAM-1 on myocytes (arrowheads) and vascular tissue (thin arrow) was seen (original magnification, ×50). The Annals of Thoracic Surgery 1997 64, 1004-1012DOI: (10.1016/S0003-4975(97)00816-3)

Fig. 3 Heart grafts from donors pretreated with lipopolysaccharide (LPS, 5 mg/kg) showed increased reperfusion injury as evidenced by (A) neutrophil infiltration, (B) cardiac edema, and (C) histologic injury (contraction band necrosis [CBN]. Recipients of LPS-pretreated grafts that were dosed with anti–intercellular adhesion molecule-1 monoclonal antibody (anti–ICAM-1 mAb, 1A29) before graft reperfusion showed baseline levels of graft reperfusion injury. (∗p < 0.05 comparing LPS-pretreated grafts with other two groups by Student’s t test.) The Annals of Thoracic Surgery 1997 64, 1004-1012DOI: (10.1016/S0003-4975(97)00816-3)

Fig. 4 Hematoxylin and eosin–stained sections of PVG grafts from lipopolysaccharide-pretreated donors procured after 90 days in ACI recipients treated with an initial 10-day course of cyclosporin A, 5 mg · kg−1 · day−1. Vessels displayed full range of vasculopathy as evidenced by the classic concentric neointimal layer central to the internal elastic laminae (arrow). Scores of individual vessels ranged from 0 (no involvement) to 4 (>50% luminal narrowing up to complete occlusion). (Original magnification, ×100.) The Annals of Thoracic Surgery 1997 64, 1004-1012DOI: (10.1016/S0003-4975(97)00816-3)