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The Journal of Thoracic and Cardiovascular Surgery, Vol 104, 1589-1596, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
JG Byrne, WJ Smith, MP Murphy, GS Couper, RF Appleyard and LH Cohn
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)
ARTICLES
Complete prevention of myocardial stunning, contracture, low-reflow, and edema after heart transplantation by blocking neutrophil adhesion molecules during reperfusion
Department of Surgery, Harvard Medical School, Boston, Mass.
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