Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants

被引:73
作者
Suzuki, T [1 ]
Fukuda, T [1 ]
Ito, T [1 ]
Inoue, Y [1 ]
Cho, Y [1 ]
Kashima, I [1 ]
机构
[1] Tokyo Metropolitan Childrens Hosp, Div Cardiovasc Surg, Tokyo 2048567, Japan
关键词
D O I
10.1016/S0003-4975(99)01332-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Lung injury after cardiopulmonary bypass is a serious complication for infants with congenital heart disease and pulmonary hypertension. Excessive neutrophil sequestration in the lung occurring after reestablishment of pulmonary circulation implies that interaction between neutrophils and pulmonary endothelium is the major cause of lung injury. Methods. Thirty infants with either ventricular septal defect or atrioventricular septal defect and with pulmonary hypertension were enrolled in this study. We performed continuous pulmonary perfusion during total cardiopulmonary bypass on 16 patients (perfused group) and conventional cardiopulmonary bypass on 14 patients (control group). PaO2/FiO(2) and neutrophil counts were assessed from immediately before surgery to 24 hours after termination of cardiopulmonary bypass. Results. PaO2/FiO(2) was higher in the perfused group than in the control group, and the difference was significant throughout the study period. Neutrophil counts decreased below prebypass values in both groups at 30 minutes after aortic unclamping, and the difference was significant in the control group but was not in the perfused group. Duration of postoperative ventilatory support was significantly less in the perfused group. Conclusions. Our study demonstrates that arrested pulmonary circulation during cardiopulmonary bypass is the major risk factor of lung injury and that continuous pulmonary perfusion is effective in preventing lung injury. (C) 2000 by The Society of Thoracic Surgeons.
引用
收藏
页码:602 / 606
页数:5
相关论文
共 26 条
[1]   ROLE OF XANTHINE-OXIDASE AND NEUTROPHILS IN ISCHEMIA-REPERFUSION INJURY IN RABBIT LUNG [J].
ADKINS, WK ;
TAYLOR, AE .
JOURNAL OF APPLIED PHYSIOLOGY, 1990, 69 (06) :2012-2018
[2]   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
[3]   INTERLEUKIN-8 RELEASE AND NEUTROPHIL DEGRANULATION AFTER PEDIATRIC CARDIOPULMONARY BYPASS [J].
FINN, A ;
NAIK, S ;
KLEIN, N ;
LEVINSKY, RJ ;
STROBEL, S ;
ELLIOTT, M .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1993, 105 (02) :234-241
[4]   ENDOTHELIAL AND MYOCARDIAL INJURY DURING ISCHEMIA AND REPERFUSION - PATHOGENESIS AND THERAPEUTIC IMPLICATIONS [J].
FORMAN, MB ;
PUETT, DW ;
VIRMANI, R .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1989, 13 (02) :450-459
[5]  
FRERING B, 1994, J THORAC CARDIOV SUR, V108, P636
[6]   Neutrophil adhesion blockade with NPC 15669 decreases pulmonary injury after total cardiopulmonary bypass [J].
Friedman, M ;
Wang, SY ;
Sellke, FW ;
Cohn, WE ;
Weintraub, RM ;
Johnson, RG .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1996, 111 (02) :460-468
[7]  
FRIEDMAN M, 1994, CIRCULATION, V90, P262
[8]   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
[9]   THROMBOXANE MEDIATES DIAPEDESIS AFTER ISCHEMIA BY ACTIVATION OF NEUTROPHIL ADHESION RECEPTORS INTERACTING WITH BASALLY EXPRESSED INTERCELLULAR-ADHESION MOLECULE .1. [J].
GOLDMAN, G ;
WELBOURN, R ;
KLAUSNER, JM ;
VALERI, CR ;
SHEPRO, D ;
HECHTMAN, HB .
CIRCULATION RESEARCH, 1991, 68 (04) :1013-1019
[10]   MEMBRANE-OXYGENATOR PREVENTS LUNG REPERFUSION INJURY IN CANINE CARDIOPULMONARY BYPASS [J].
GU, YJ ;
WANG, YS ;
CHIANG, BY ;
GAO, XD ;
YE, CX ;
WILDEVUUR, CRH .
ANNALS OF THORACIC SURGERY, 1991, 51 (04) :573-578