Increased leukocyte-platelet adhesion in patients with graft occlusion after peripheral vascular surgery

被引:21
作者
Esposito, CJ
Popescu, WM
Rinder, HM
Schwartz, JJ
Smith, BR
Rinder, CS
机构
[1] Yale Univ, Sch Med, Dept Anesthesiol, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06520 USA
关键词
cell-cell interactions; clinical/epidemiological studies; platelet activation markers; vasculopathies;
D O I
10.1160/TH03-04-0226
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Graft occlusion following peripheral vascular surgery is attributable to some combination of acute thrombosis, and progression of atherosclerosis: interactions between leukocytes and activated platelets may play a role in both of these processes. This investigation measured perioperative leukocyte-platelet conjugate formation, and leukocyte and platelet activation in 46 patients undergoing surgery for lower extremity peripheral vascular disease (PVD). All patients were followed for graft patency over the next 6 months; 27 patients had grafts that remained patent while 19 had graft occlusion. On postoperative day #1 (POW), the graft occlusion group demonstrated a significantly greater increase in circulating levels of both monocyteplatelet and neutrophil (PMN)-platelet conjugates compared to the patent graft patients (p=0.015 and 0.018, respectively). PMN activation, assessed by increases in surface CDI lb expression, was also significantly increased on POD#l in the graft occlusion group compared to the patent group (p=0.026). The percentage of circulating activated (CD62P+) platelets did not differ between groups, but patients with graft occlusion demonstrated a higher percentage of younger, reticulated platelets throughout the study period (p=0.008), indicating increased platelet turnover. We conclude that in the early postoperative period, leukocyte-platelet adhesion, PMN activation, and platelet turnover are significantly greater in PVD patients who go on to develop later graft occlusion. Cellular activation and heterotypic cell interactions in peripheral vascular surgery patients may be important in the etiologies of thrombosis and/or accelerated atherosclerosis leading to graft loss.
引用
收藏
页码:1128 / 1134
页数:7
相关论文
共 47 条
[1]   THE SIGNIFICANCE OF PLATELETS WITH INCREASED RNA-CONTENT (RETICULATED PLATELETS) - A MEASURE OF THE RATE OF THROMBOPOIESIS [J].
AULT, KA ;
RINDER, HM ;
MITCHELL, J ;
CARMODY, MB ;
VARY, CPH ;
HILLMAN, RS .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1992, 98 (06) :637-646
[2]   DETERMINATION OF THE PERCENTAGE OF THIAZOLE ORANGE (TO)-POSITIVE, RETICULATED PLATELETS USING AUTOLOGOUS ERYTHROCYTE TO FLUORESCENCE AS AN INTERNAL STANDARD [J].
BONAN, JL ;
RINDER, HM ;
SMITH, BR .
CYTOMETRY, 1993, 14 (06) :690-694
[3]   Neutrophil reactive oxygen species production during hemodialysis: Role of activated platelet adhesion to neutrophils through P-selectin [J].
Bonomini, M ;
Stuard, S ;
Carreno, MP ;
Settefrati, N ;
Santarelli, P ;
HaeffnerCavaillon, N ;
Albertazzi, A .
NEPHRON, 1997, 75 (04) :402-411
[4]   Preoperative thromboxane A2/prostaglandin H2 receptor activity predicts early graft thrombosis [J].
Brothers, TE ;
Robison, JG ;
Elliott, BM ;
Boggs, JM .
JOURNAL OF VASCULAR SURGERY, 1998, 27 (02) :317-325
[5]  
Brunetti M, 2000, THROMB HAEMOSTASIS, V84, P478
[6]   Epidemiology and pathophysiology [J].
Cimminiello, C .
THROMBOSIS RESEARCH, 2002, 106 (06) :V295-V301
[7]  
CONSTANTINI V, 2002, THROMB RES, V106, pV285
[8]   Platelet/polymorphonuclear leukocyte interaction: P-selectin triggers protein-tyrosine phosphorylation-dependent CD11b/CD18 adhesion: Role of PSGL-1 as a signaling molecule [J].
Evangelista, V ;
Manarini, S ;
Sideri, R ;
Rotondo, S ;
Martelli, N ;
Piccoli, A ;
Totani, L ;
Piccardoni, P ;
Vestweber, D ;
de Gaetano, G ;
Cerletti, C .
BLOOD, 1999, 93 (03) :876-885
[9]   Platelet-monocyte aggregates - Bridging thrombosis and inflammation [J].
Freedman, JE ;
Loscalzo, J .
CIRCULATION, 2002, 105 (18) :2130-2132
[10]   Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction [J].
Furman, MI ;
Barnard, MR ;
Krueger, LA ;
Fox, ML ;
Shilale, EA ;
Lessard, DM ;
Marchese, P ;
Frelinger, AL ;
Goldberg, RJ ;
Michelson, AD .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2001, 38 (04) :1002-1006