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J Thorac Cardiovasc Surg 1998;116:114-118
© 1998 Mosby, Inc.

Cardiopulmonary Support And Physiology

Inhibition Of Interleukin-8 Blocks Myocardial Ischemia-Reperfusion Injury

Funded in part by the 3M/Surgical Infection Society Resident Research Fellowship (E. M. B.), the Thoracic Surgery Foundation for Research and Education Fellowship (E. M. B.), and the National Institutes of Health grants GM 46662 and T32 GM 07037 (T.  H. P.).

Read at the Twenty-third Annual Meeting of The Western Thoracic Surgical Association, Napa, Calif., June 25-28, 1997.

Address for reprints: Edward D. Verrier, MD, Professor and Chief, Division of Cardiothoracic Surgery, University of Washington, 1959 Pacific Ave. N.E., Box 356310, Seattle, WA 98195.

Introduction: Interleukin-8 is thought to play a role in neutrophil activation and transcapillary migration into the interstitium. Because neutrophils are principal effector cells in acute myocardial ischemia-reperfusion injury, we postulated that the inhibition of interleukin-8 activity with a neutralizing monoclonal antibody directed against rabbit interleukin-8 (ARIL8.2) would attenuate the degree of myocardial injury encountered during reperfusion.
Methods: In New Zealand White rabbits, the large branch of the marginal coronary artery supplying most of the left ventricle was occluded for 45 minutes, followed by 2 hours of reperfusion. Fifteen minutes before reperfusion, animals were given an intravenous bolus of either 2 mg/kg of ARIL8.2 or 2 mg/kg anti–glycoprotein-120, an isotype control antibody that does not recognize interleukin-8. At the completion of the 120-minute reperfusion period, infarct size was determined.
Results: In the area at risk for infarction, 44.3% ± 4% of the myocardium was infarcted in the anti–glycoprotein-120 group compared with 24.8% ± 9% in the ARIL8.2 group (p < 0.005). In control animals, edema and diffuse infiltration of neutrophils were observed predominantly in the infarct zone and the surrounding area at risk. Tissue myeloperoxidase determinations did not differ significantly between groups, indicating that the cardioprotective effect of ARIL8.2 was independent of an effect on neutrophil infiltration.
Conclusions: A specific monoclonal antibody that neutralizes interleukin-8 significantly reduces the degree of necrosis in a rabbit model of myocardial ischemia-reperfusion injury.

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