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The relationship between neutrophils and increased microvascular permeability in a model of myocardial ischaemia and reperfusion in the rabbit
Author(s) -
Williams Frances M.,
Collins Paul D.,
TannièreZeller Marianne,
Williams Timothy J.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14083.x
Subject(s) - albumin , ischemia , evans blue , medicine , platelet activating factor , coronary occlusion , vascular permeability , chemistry , endocrinology , antagonist , pharmacology , receptor
1 111 In‐labelled neutrophils and 125 I‐labelled albumin were used to measure neutrophil accumulation and microvascular plasma protein leakage in the ischaemic/reperfused myocardium of anaesthetized rabbits. 2 A period of 30 min coronary artery occlusion followed by 3h reperfusion resulted in an increase in both 111 In and 125 I counts in the area at risk (AR) of the myocardium. 3 Pretreatment of 111 In‐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. 4 Depletion of circulating neutrophils by use of anti‐neutrophil serum or mustine hydrochloride did not affect plasma protein leakage into the AR myocardium. 5 Administration of the platelet activating factor (PAF) antagonist WEB 2086 (10 mg kg −1 , i.v.) had no effect on the accumulation of 111 In‐neutrophils or on plasma protein leakage in the AR myocardium.