Neutrophils are the initial cell type identified in deep venous thrombosis induced vein wall inflammation

被引:46
作者
Downing, LJ
Strieter, RM
Kadell, AM
Wilke, CA
Brown, SL
Wrobleski, SK
Burdick, MD
Hulin, MS
Fowlkes, JB
Greenfield, LJ
Wakefield, TW
机构
[1] UNIV MICHIGAN,DEPT SURG,VASC SURG SECT,ANN ARBOR,MI 48109
[2] UNIV MICHIGAN,DEPT SURG,JOBST VASC RES LAB,ANN ARBOR,MI 48109
[3] UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109
[4] UNIV MICHIGAN,DEPT RADIOL,ANN ARBOR,MI 48109
[5] VET ADM MED CTR,ANN ARBOR,MI
关键词
D O I
10.1097/00002480-199609000-00073
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Venous thrombosis and inflammation are interrelated. The authors hypothesized that inferior vena cava thrombosis results in a predictable vein wall inflammatory response, characterized by early neutrophil infiltration. Thrombosis was induced in rats by placement of an inferior vena cave ligature with branch ligation. Animals were killed at baseline, 6 hrs, day 2, and day 6. Analysis included vein wall morphometrics, myeloperoxidase activity, and fluorescence activated cell sorting. At 6 hrs, there was an increase in neutrophils and lymphocytes as compared to sham animals (p < 0.0001 for neutrophils, p < 0.05 for lymphocytes). By day 2, only neutrophils were elevated in the experimental groups (experimental = 75.5 cells/5 high power fields vs. 9.6 cells/5 high power fields in shams, p < 0.0001). Myeloperoxidase activity in the experimental group was greater than shams on day 2 (34.7 Delta optical density/min vs. 5.9 Delta optical density/min, p < 0.0001). Fluorescence activated cell sorting of the neutrophil marker at 6 hrs confirmed the increase in neutrophils (experimental = 63.1%, shams = 39.1%, p < 0.0001), and peaked on day 2 (71.9%). This study suggests that 1) neutrophils are elevated early during the inflammatory response due to thrombus initiation, and 2) neutrophils, because of their early predominance, likely contributed to vein wall injury during venous thrombosis.
引用
收藏
页码:M677 / M682
页数:6
相关论文
共 32 条
[1]  
ARENBERG DA, IN PRESS J CLIN INVE
[2]  
BAGGIOLINI M, 1994, ADV IMMUNOL, V55, P97
[3]   NEUTROPHIL-ACTIVATING PEPTIDE-1 INTERLEUKIN-8, A NOVEL CYTOKINE THAT ACTIVATES NEUTROPHILS [J].
BAGGIOLINI, M ;
WALZ, A ;
KUNKEL, SL .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (04) :1045-1049
[4]   EPIDEMIOLOGY OF CHRONIC VENOUS ULCERS [J].
BAKER, SR ;
STACEY, MC ;
JOPPMCKAY, AG ;
HOSKIN, SE ;
THOMPSON, PJ .
BRITISH JOURNAL OF SURGERY, 1991, 78 (07) :864-867
[5]   POLYMORPHONUCLEAR LEUKOCYTE INFILTRATION INTO CEREBRAL FOCAL ISCHEMIC TISSUE - MYELOPEROXIDASE ACTIVITY ASSAY AND HISTOLOGIC VERIFICATION [J].
BARONE, FC ;
HILLEGASS, LM ;
PRICE, WJ ;
WHITE, RF ;
LEE, EV ;
FEUERSTEIN, GZ ;
SARAU, HM ;
CLARK, RK ;
GRISWOLD, DE .
JOURNAL OF NEUROSCIENCE RESEARCH, 1991, 29 (03) :336-345
[6]   A PLATELET ALPHA GRANULE MEMBRANE-PROTEIN THAT IS ASSOCIATED WITH THE PLASMA-MEMBRANE AFTER ACTIVATION - CHARACTERIZATION AND SUBCELLULAR-LOCALIZATION OF PLATELET ACTIVATION-DEPENDENT GRANULE-EXTERNAL MEMBRANE-PROTEIN [J].
BERMAN, CL ;
YEO, EL ;
WENCELDRAKE, JD ;
FURIE, BC ;
GINSBERG, MH ;
FURIE, B .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 78 (01) :130-137
[7]  
BONFANTI R, 1989, BLOOD, V73, P1109
[8]   LEUKOCYTE-ENDOTHELIAL CELL RECOGNITION - 3 (OR MORE) STEPS TO SPECIFICITY AND DIVERSITY [J].
BUTCHER, EC .
CELL, 1991, 67 (06) :1033-1036
[9]   CHEMOKINE EXPRESSION DURING HEPATIC ISCHEMIA REPERFUSION-INDUCED LUNG INJURY IN THE RAT [J].
COLLETTI, LM ;
KUNKEL, SL ;
WALZ, A ;
BURDICK, MD ;
KUNKEL, RG ;
WILKE, CA ;
STRIETER, RM .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (01) :134-141
[10]   VENOUS THROMBOEMBOLISM AND OTHER VENOUS DISEASE IN TECUMSEH-COMMUNITY-HEALTH-STUDY [J].
COON, WW ;
WILLIS, PW ;
KELLER, JB .
CIRCULATION, 1973, 48 (04) :839-846