Document Detail

CD18 antibody treatment limits early myocardial reperfusion injury after initial leukocyte deposition.
MedLine Citation:
PMID:  8812625     Owner:  NLM     Status:  MEDLINE    
Following myocardial ischemia, initial reperfusion with whole blood impairs the recovery of ventricular function. The exact mechanisms underlying early myocardial reperfusion injury are not clear, but leukocytes play an important role. In this study, we tested if treating the initial blood reperfusate with a monoclonal antibody (CL26) against the leukocyte adhesion protein (CD18 would reduce the leukocyte contribution to early reperfusion injury. We reasoned that blocking CD18 would reduce the initial retention of leukocytes in the heart and thereby limit the inflammatory response. Rat hearts were isolated and perfused at constant flow with a red cell-rich solution (K2RBC). The perfusate was not recirculated. Baseline measures were made of coronary flow, perfusion pressure, and ventricular pump function. No-flow, normothermic ischemia was induced for 30 min, followed immediately by reperfusion, at the preischemic flowrate, with diluted whole blood (DWB, treated with either vehicle or CL26). Reperfusion was continued with K2RBC for 40 min more, during which postischemic measures were made. We found that the cardiac retention of leukocytes was not significantly different for the two groups, nor were the recoveries of ventricular function. Later in reperfusion (R35), the coronary blood flowrate and the coronary vascular resistances were not different; however, the recoveries of ventricular pump function were significantly different (+dP/dt @ R35 (%Pre-I): Vehicle: 27 +/- 9% (n = 8); CL26: 51 +/- 6% (n = 7); P < 0.05). Also, at R35, the voltage required to capture and pace the vehicle-treated hearts was significantly greater than the voltage required to pace the CL26 hearts (P < 0.05). Because the coronary flowrate and leukocyte retention were similar for both groups, the improved recovery observed in the CL26-treated group was not due to either improved flow or to reduced leukocyte retention. Rather, the findings suggest that the beneficial effect of antibody treatment was to attenuate step(s) in the acute inflammatory response that occurred after the initial deposition of leukocytes in the heart.
P F McDonagh; D S Wilson; H Iwamura; C W Smith; S K Williams; J G Copeland
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of surgical research     Volume:  64     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-10-21     Completed Date:  1996-10-21     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  139-49     Citation Subset:  IM    
Department of Surgery, College of Medicine, University of Arizona, Tucson, USA.
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MeSH Terms
Antibodies, Monoclonal / pharmacology*
Antigens, CD18 / immunology*
Blood Pressure / physiology
Coronary Vessels / immunology*
Heart Ventricles / surgery
Hemodynamics / physiology
Leukocyte Count
Leukocytes / cytology,  physiology*
Muscle Contraction / physiology
Muscle Fibers, Skeletal / physiology
Myocardial Reperfusion Injury / drug therapy*,  surgery
Pacemaker, Artificial
Rats, Sprague-Dawley
Vascular Resistance / physiology
Ventricular Function
Ventricular Function, Left / physiology
Grant Support
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antigens, CD18

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