Enhanced isolated lung function after ischemia with anti-intercellular adhesion molecule antibody

被引:9
作者
Buchanan, SA [1 ]
Mauney, MC [1 ]
deLima, NF [1 ]
Binns, OAR [1 ]
Cope, JS [1 ]
Shockey, KS [1 ]
Gordon, SG [1 ]
Erwin, MB [1 ]
Sutherland, G [1 ]
Kron, IL [1 ]
Tribble, CG [1 ]
机构
[1] UNIV VIRGINIA,HLTH SCI CTR,DEPT SURG,THORAC & CARDIOVASC RES LAB,CHARLOTTESVILLE,VA 22908
关键词
D O I
10.1016/S0022-5223(96)70368-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The binding of leukocytes to intercellular adhesion molecules expressed on endothelial surfaces during ischemia and subsequent reperfusion initiates leukocyte-mediated reperfusion injury. Interruption of this leukocyte-endothelium interaction may therefore prevent reperfusion injury. In an isolated, ventilated, blood-perfused rabbit lung preparation, we studied the effect of a monoclonal anti-intercellular adhesion molecule antibody on lung function during reperfusion. Lungs were harvested with 50 ml/kg cold Euro-Collins flush add 30 mu g prostaglandin E(1) before storage for 18 hours at 4 degrees C. Experimental groups received low-dose (100 mu g) or high-dose (200 mu g) anti-intercellular adhesion molecule antibody added to the pulmonary flush at harvest and to the initial reperfusate. Eighteen-hour control preparations were preserved for 18 hours and received saline solution vehicle. Immediate control preparations were harvested and immediately reperfused. The oxygen tension in the recirculated pulmonary venous effluent was measured after 30 minutes of reperfusion. Histologic specimens were graded by blinded observers for degree of leukocyte infiltration (0, normal, to 4, severe infiltration). The mean oxygen tensions (+/-standard error of the mead) were 138.29 +/- 6.23, 58.86 +/- 9.14, 86.87 +/- 11.32, and 139.33 +/- 16.15 mm Hg in immediate control preparations, 18-hour control preparations, low-dose antibody group, and high-dose antibody group, respectively (p = 0.0001). The leukocyte grades (mean +/- standard error of the mead) were 1.5 +/- 0.723, 3.0 +/- 0.955, 1.9 +/- 0.899, and 1.2 +/- 0.834, respectively (p = 0.0002). We conclude that anti-intercellular adhesion molecule antibody added to the pulmonary flush and initial reperfusate results in a dose-dependent enhancement of the reperfused lung's ability to oxygenate blood, possibly as a result of decreased leukocyte sequestration.
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收藏
页码:941 / 946
页数:6
相关论文
共 23 条
[1]  
BANDO K, 1991, J HEART LUNG TRANSPL, V10, P304
[2]  
BANDO K, 1990, J THORAC CARDIOV SUR, V99, P873
[3]   MONOCLONAL-ANTIBODY TO THE ICAM-1 ADHESION SITE REDUCES NEUROLOGICAL DAMAGE IN A RABBIT CEREBRAL EMBOLISM STROKE MODEL [J].
BOWES, MP ;
ZIVIN, JA ;
ROTHLEIN, R .
EXPERIMENTAL NEUROLOGY, 1993, 119 (02) :215-219
[4]   COMPLETE PREVENTION OF MYOCARDIAL STUNNING, CONTRACTURE, LOW-REFLOW, AND EDEMA AFTER HEART-TRANSPLANTATION BY BLOCKING NEUTROPHIL ADHESION MOLECULES DURING REPERFUSION [J].
BYRNE, JG ;
SMITH, WJ ;
MURPHY, MP ;
COUPER, GS ;
APPLEYARD, RF ;
COHN, LH .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1992, 104 (06) :1589-1596
[5]   REDUCTION OF CENTRAL-NERVOUS-SYSTEM ISCHEMIC-INJURY IN RABBITS USING LEUKOCYTE ADHESION ANTIBODY TREATMENT [J].
CLARK, WM ;
MADDEN, KP ;
ROTHLEIN, R ;
ZIVIN, JA .
STROKE, 1991, 22 (07) :877-883
[6]  
DICKSTEIN RA, 1990, PERFUSION LIFE, V7, P34
[7]   INHIBITION OF NEUTROPHIL ADHESION DURING CARDIOPULMONARY BYPASS [J].
GILLINOV, AM ;
REDMOND, JM ;
ZEHR, KJ ;
WILSON, IC ;
CURTIS, WE ;
BATOR, JM ;
BURCH, RM ;
REITZ, BA ;
BAUMGARTNER, WA ;
HERSKOWITZ, A ;
CAMERON, DE .
ANNALS OF THORACIC SURGERY, 1994, 57 (01) :126-133
[8]  
GORLICK DL, 1992, P AM AC CAR, V13, P154
[9]   A PHASE-I TRIAL OF IMMUNOSUPPRESSION WITH ANTI-ICAM-1 (CD54) MAB IN RENAL-ALLOGRAFT RECIPIENTS [J].
HAUG, CE ;
COLVIN, RB ;
DELMONICO, FL ;
AUCHINCLOSS, H ;
TOLKOFFRUBIN, N ;
PREFFER, FI ;
ROTHLEIN, R ;
NORRIS, S ;
SCHARSCHMIDT, L ;
COSIMI, AB ;
BARKER ;
HARDY ;
TESI ;
KAHAN .
TRANSPLANTATION, 1993, 55 (04) :766-773
[10]   ROLE OF ICAM-1 IN NEUTROPHIL-MEDIATED LUNG VASCULAR INJURY AFTER OCCLUSION AND REPERFUSION [J].
HORGAN, MJ ;
MING, G ;
JIANG, G ;
ROTHLEIN, R ;
MALIK, AB .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (05) :H1578-H1584