Nitric oxide inhibits neutrophil adhesion during experimental extracorporeal circulation

被引:34
作者
Chello, M
Mastroroberto, P
Marchese, AR
Maltese, G
Santangelo, E
Amantea, B
机构
[1] Med Sch Catanzaro, Dept Cardiac Surg, Catanzaro, Italy
[2] Med Sch Catanzaro, Dept Anesthesiol, Catanzaro, Italy
关键词
adhesion; cardiopulmonary bypass; neutrophils; nitric oxide;
D O I
10.1097/00000542-199808000-00021
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background Myocardial and pulmonary Injuries often occur after cardiopulmonary bypass, mediated in part by neutrophil activation and adhesion to endothelial cells. The effects of nitric oxide (NO) administration on neutrophil adhesion to endothelial cells after simulated extracorporeal circulation were investigated. Methods: Two identical extracorporeal circulation circuits were primed with fresh human blood and circulated for 2 h at 37 degrees C. Nitric oxide at a 40-ppm concentration was added to one of the oxygenators in each pair. Neutrophil CD11b/CD18 expression and their adhesion to human umbilical vein endothelial cell monolayers were assayed in leukocytes isolated from samples drawn from the circuit 30, 60, 90, and 120 min after circulation began. in another series of experiments, blocking monoclonal antibodies to both neutrophil CD11b and CD18 were incubated with polymorphonuclear leukocytes after removal from the circuit before the adhesion assay. Results: After 60 min of circulation, the neutrophils from NO-treated circuits showed significantly reduced CD11b/CD18 surface expression compared with the control group. There was also a significant reduction in neutrophil-endothelial adhesion in the NO group after 120 min of circulation. Monoclonal antibodies to both CD11b and CD18 significantly inhibited the adhesion of polymorphonuclear leukocytes at endothelial cells after 120 min of circulation. Conclusions: These results confirm that neutrophil activation occurs during cardiopulmonary bypass. The addition of NO to the circuits of extracorporeal circulation significantly affects neutrophil adhesion to endothelial cells.
引用
收藏
页码:443 / 448
页数:6
相关论文
共 23 条
[1]   INFLAMMATORY RESPONSE TO CARDIOPULMONARY BYPASS [J].
BUTLER, J ;
ROCKER, GM ;
WESTABY, S .
ANNALS OF THORACIC SURGERY, 1993, 55 (02) :552-559
[2]  
CARLOS TM, 1994, BLOOD, V84, P2068
[3]   COMPLEMENT ACTIVATION DURING CARDIOPULMONARY BYPASS - EVIDENCE FOR GENERATION OF C3A AND C5A ANAPHYLATOXINS [J].
CHENOWETH, DE ;
COOPER, SW ;
HUGLI, TE ;
STEWART, RW ;
BLACKSTONE, EH ;
KIRKLIN, JW .
NEW ENGLAND JOURNAL OF MEDICINE, 1981, 304 (09) :497-503
[4]   INTERACTION BETWEEN NEUTROPHILS AND ENDOTHELIUM [J].
ELLIOTT, MJ ;
FINN, AHR .
ANNALS OF THORACIC SURGERY, 1993, 56 (06) :1503-1508
[5]   PREPARATIVE PROCEDURES OF COOLING AND REWARMING INCREASE LEUKOCYTE INTEGRIN EXPRESSION AND FUNCTION ON NEUTROPHILS [J].
FORSYTH, KD ;
LEVINSKY, RJ .
JOURNAL OF IMMUNOLOGICAL METHODS, 1990, 128 (02) :159-163
[6]   NITRIC-OXIDE PREVENTS LEUKOCYTE ADHERENCE - ROLE OF SUPEROXIDE [J].
GABOURY, J ;
WOODMAN, RC ;
GRANGER, DN ;
REINHARDT, P ;
KUBES, P .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (03) :H862-H867
[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]   The systemic inflammatory response to cardiopulmonary bypass: Pathophysiological, therapeutic, and pharmacological considerations [J].
Hall, RI ;
Smith, MS ;
Rocker, G .
ANESTHESIA AND ANALGESIA, 1997, 85 (04) :766-782
[9]   NITROVASODILATORS INHIBIT THROMBIN-INDUCED PLATELET-ACTIVATING-FACTOR SYNTHESIS IN HUMAN ENDOTHELIAL-CELLS [J].
HELLER, R ;
BUSSOLINO, F ;
GHIGO, D ;
GARBARINO, G ;
PESCARMONA, G ;
TILL, U ;
BOSIA, A .
BIOCHEMICAL PHARMACOLOGY, 1992, 44 (02) :223-229
[10]   Inflammatory cascade - A final common pathway for perioperative injury [J].
Herskowitz, A ;
Mangano, DT .
ANESTHESIOLOGY, 1996, 85 (05) :957-960