THE RELATIONSHIP BETWEEN NEUTROPHILS AND INCREASED MICROVASCULAR PERMEABILITY IN A MODEL OF MYOCARDIAL-ISCHEMIA AND REPERFUSION IN THE RABBIT

111In-labelled neutrophils and 125I-labelled albumin were used to measure neutrophil accumulation and microvascular plasma protein leakage in the ischaemic/reperfused myocardium of anaesthetized rabbits. A period of 30 min coronary artery occlusion followed by 3 h reperfusion resulted in an increase in both 111In and 125I counts in the area at risk (AR) of the myocardium. Pretreatment of 111In-neutrophils in vitro with monoclonal antibody 60.3 directed against the CD18 antigen on neutrophils, followed by intravenous administration, significantly suppressed their accumulation into the AR myocardium. Depletion of circulating neutrophils by use of anti-neutrophil serum or mustine hydrochloride did not affect plasma protein leakage into the AR myocardium. Administration of the platelet activating factor (PAF) antagonist WEB 2086 (10 mg kg-1, i.v.) had no effect on the accumulation of 111In-neutrophils or on plasma protein leakage in the AR myocardium.