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Diltiazem at reperfusion reduces neutrophil accumulation and infarct size in dogs with ischaemic myocardium
Study objective – The aim was to demonstrate the ability of diltiazem to protect the ischaemic myocardium in the course of coronary reperfusion, and to establish if an interaction with neutrophils is implied. Design – Ischaemia was induced by occluding the left anterior descending coronary artery fo...
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Published in: | Cardiovascular research 1991-04, Vol.25 (4), p.319-329 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Study objective – The aim was to demonstrate the ability of diltiazem to protect the ischaemic myocardium in the course of coronary reperfusion, and to establish if an interaction with neutrophils is implied. Design – Ischaemia was induced by occluding the left anterior descending coronary artery for 90 min followed by 6 h of reperfusion with a residual critical stenosis left in place. Three groups were studied: group 1 (control) received a saline perfusion; group 2 was given a bolus injection of 400 μg·kg−1 of diltiazem 10 min before reperfusion, followed by 4 μg·kg_1-min_1 perfusion until termination of experiment; group 3 was made neutropenic by injecting a neutrophil antiserum produced in rabbits and was then treated with diltiazem, as in the second group. Subjects – 60 mongrel dogs of either sex were allocated at random into one of the three groups the day before the experiment. Measurements and main results – Diltiazem plasma concentrations ranged from 68.6(SEM 10.0) to 102.5(15.2) μg·litre−1 during the study. Transmural collateral blood flow, measured with 153Gd microspheres 15 min after occlusion, and area at risk, evaluated by Evans blue perfusion, did not differ among the three groups. Infarct size, estimated by triphenyltetrazoiium staining of heart slices and expressed as a percentage of area at risk, was less (p |
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ISSN: | 0008-6363 1755-3245 |
DOI: | 10.1093/cvr/25.4.319 |