Document Detail

Complete prevention of myocardial stunning, contracture, low-reflow, and edema after heart transplantation by blocking neutrophil adhesion molecules during reperfusion.
MedLine Citation:
PMID:  1360556     Owner:  NLM     Status:  MEDLINE    
This study tested the hypothesis that preventing neutrophil adhesion during reperfusion, by blocking either the neutrophil membrane CD18 integrin complex or its endothelial and myocyte ligand, intercellular adhesion molecule-1 (ICAM-1), would reduce myocardial inflammation and edema and improve reflow and ventricular function after heart preservation and transplantation. After cardioplegia and insertion of a left ventricular balloon, rabbit hearts were heterotopically transplanted into recipient rabbits either immediately (immediate, n = 12) or after preservation in 4 degrees C saline (3 hours of ischemia, n = 33). Forty-five minutes before reperfusion, recipients of preserved hearts received intravenous infusions of either saline (vehicle, n = 13), anti-CD18 monoclonal antibody (Mab) R15.7 (2 mg/kg) (anti-CD18, n = 10), or anti-ICAM-1 Mab R1.1 (2 mg/kg) (anti-ICAM, n = 10). During 3 hours of reperfusion the slope of the peak-systolic pressure-volume relation and its volume-axis intercept, the exponential elastic coefficient of the end-diastolic pressure-volume relation, the unstressed ventricular volume, and the time constant of the exponential left ventricular pressure decay after dP/dtmin were serially measured. Myocardial blood flow was measured with microspheres from which coronary vascular resistance was calculated. After explanation, the degree of myocardial inflammation, estimated by tissue neutrophil sequestration (myeloperoxidase assay) and myocardial water content were determined. Within each group no significant differences in measurements made at 1, 2, and 3 hours of reperfusion were noted. Compared with the immediate transplantation group, the vehicle group demonstrated a significant increase in myeloperoxidase activity (3380 +/- 456 versus 1712 +/- 552 microU/gm, p < 0.05), coronary vascular resistance (115.5 +/- 13.4 versus 70.5 +/- 10.6 U/gm, p < 0.05), and myocardial water content (79.8% +/- 0.4% versus 75.6% +/- 1.3%, p < 0.05), a significant decrease in unstressed ventricular volume (a leftward shift in the end-diastolic pressure-volume relation) (-0.49 +/- 0.24 versus 0.28 +/- 0.21 ml, p < 0.05), and a marked prolongation in exponential left ventricular pressure delay after dP/dtmin (156.64 +/- 3.81 versus 37.25 +/- 3.34 msec, p < 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
J G Byrne; W J Smith; M P Murphy; G S Couper; R F Appleyard; L H Cohn
Related Documents :
848436 - Acute blood pressure elevation and ventricular fibrillation threshold during coronary o...
14597146 - Peroxynitrite in reperfusion arrhythmias and its whole blood chemiluminescence results.
1984866 - Mechanism of early ischemic contractile failure. inexcitability, metabolite accumulatio...
12643846 - K(atp) channel opener protects neonatal rabbit heart better than st. thomas' solution.
6284506 - The pressure dependence of the spin equilibrium in camphor-bound ferric cytochrome p-450.
15071436 - Renal revascularization in takayasu arteritis-induced renal artery stenosis.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  104     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  1992 Dec 
Date Detail:
Created Date:  1993-01-06     Completed Date:  1993-01-06     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1589-96     Citation Subset:  AIM; IM    
Department of Surgery, Harvard Medical School, Boston, Mass.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antibodies, Monoclonal / pharmacology*,  therapeutic use
Antigens, CD / drug effects*
Antigens, CD18
Cardiomyopathies / prevention & control
Cell Adhesion Molecules / drug effects*
Coronary Circulation
Edema / prevention & control
Heart Transplantation / immunology,  physiology*
Inflammation / prevention & control
Integrins / drug effects*
Intercellular Adhesion Molecule-1
Myocardial Reperfusion Injury / prevention & control*
Neutrophils / drug effects,  physiology
Organ Preservation / methods*
Receptors, Leukocyte-Adhesion / drug effects*
Transplantation, Heterotopic
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antigens, CD; 0/Antigens, CD18; 0/Cell Adhesion Molecules; 0/Integrins; 0/Receptors, Leukocyte-Adhesion; 126547-89-5/Intercellular Adhesion Molecule-1

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

Previous Document:  Mesangial cell killing by leukocytes: role of leukocyte oxidants and proteolytic enzymes.
Next Document:  Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable...