Document Detail

Lung reperfusion injury is reduced by inhibiting a CD18-dependent mechanism.
MedLine Citation:
PMID:  8097405     Owner:  NLM     Status:  MEDLINE    
CD18 designates a component of a leukocyte surface glycoprotein complex that mediates endothelial adherence. To determine whether interference with CD18-dependent leukocyte adhesion modifies reperfusion injury, we transplanted 16 canine left lungs after 4-hour preservation with modified Euro-Collins solution. Anti-canine CD18 monoclonal antibody (R15.7, 1 mg/kg, intravenously) was administered to eight lung recipients 5 minutes before reperfusion; eight control recipients were not treated. Ventilation was identical in donor-recipient pairs (tidal volume, 600 ml; fraction of inspired oxygen, 0.53; positive end-expiratory pressure, 5 cm H2O). Respiratory and inert gas exchange and hemodynamics were assessed in left lung donors one-half hour after right lung exclusion and in allograft recipients at 0.5, 1.5, 2.5, 3.5, and 6.0 hours after transplantation and right lung exclusion. Reperfusion injury was evident in both recipient groups at 6 hours after transplantation, but inert gas shunt was lower in monoclonal antibody-treated dogs (13% +/- 6%) than in controls (30% +/- 17%, p < 0.05); comparisons of arterial blood gases in monoclonal antibody recipients (PaO2, 209 +/- 83 mm Hg; PaCO2, 45 +/- 7 mm Hg) and controls (PaO2, 108 +/- 54, p < 0.05; PaCO2, 64 +/- 25, p < 0.05) at 6 hours indicated that monoclonal antibody administration distinctly improved respiratory gas transfer. Gravimetric lung water was less in monoclonal antibody recipients (5.78 +/- 1.01 ml/kg) than in controls (8.02 +/- 1.90 ml/kg, p < 0.05), but lung compliance at 6 hours was equally reduced in monoclonal antibody recipients (40 +/- 9 ml/cm H2O) and in controls (39 +/- 7 ml/cm H2O, p = not significant). Pulmonary vascular resistance doubled immediately after transplantation but was identical in monoclonal antibody-treated dogs (890 +/- 168 and in controls (874 +/- 162, p = not significant) at 6 hours. We conclude that inhibition of CD18-dependent leukocyte function attenuates the development of both shunt and abnormal respiratory gas exchange in lung reperfusion injury. Significant physiologic abnormalities occurred despite R15.7 treatment and may represent inadequate preservation or the effect of CD18-independent adhesion mechanisms.
D P Kapelanski; A Iguchi; S D Niles; H Z Mao
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation     Volume:  12     ISSN:  1053-2498     ISO Abbreviation:  J. Heart Lung Transplant.     Publication Date:    1993 Mar-Apr
Date Detail:
Created Date:  1993-05-26     Completed Date:  1993-05-26     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  9102703     Medline TA:  J Heart Lung Transplant     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  294-306; discussion 306-7     Citation Subset:  IM    
Department of Surgery, University of Iowa College of Medicine, Iowa City.
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MeSH Terms
Antigens, CD / physiology*
Antigens, CD18
Lung / physiopathology*
Lung Compliance
Lung Transplantation*
Pulmonary Gas Exchange
Receptors, Leukocyte-Adhesion / physiology
Reperfusion Injury / physiopathology*,  prevention & control
Ventilation-Perfusion Ratio
Reg. No./Substance:
0/Antigens, CD; 0/Antigens, CD18; 0/Receptors, Leukocyte-Adhesion

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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