Lignocaine in experimental myocardial infarction: failure to prevent neutrophil accumulation and ventricular fibrillation and to reduce infarct size

Growing evidence supports the concept that neutrophils accumulating in reperfused ischaemic myocardium play a detrimental role in evolving infarction. Lignocaine, an antiarrhythmic drug commonly used clinically, interferes with neutrophil function in vitro and potentially in vivo. To test the hypoth...

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Bibliographic Details
Published in:Cardiovascular research 1988-06, Vol.22 (6), p.439-446
Main Authors: LORGERIL, MICHEL DE, ROUSSEAU, GUY, BASMADJIAN, ARSENE, LATOUR, JEAN-GILLES
Format: Article
Language:English
Subjects:
Animals
Antiarythmic agents
Biological and medical sciences
Cardiovascular system
coronary occlusion
Dogs
Female
Heart - diagnostic imaging
ischaemia
Leukocyte Count
Lidocaine - adverse effects
Lidocaine - therapeutic use
lignocaine
Male
Medical sciences
Myocardial Infarction - diagnostic imaging
Myocardial Infarction - drug therapy
Myocardial Infarction - pathology
Myocardium - pathology
neutrophil
Neutrophils - drug effects
Pharmacology. Drug treatments
Radionuclide Imaging
ventricular fibrillation
Ventricular Fibrillation - chemically induced
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Summary:Growing evidence supports the concept that neutrophils accumulating in reperfused ischaemic myocardium play a detrimental role in evolving infarction. Lignocaine, an antiarrhythmic drug commonly used clinically, interferes with neutrophil function in vitro and potentially in vivo. To test the hypothesis that lignocaine may influence infarct size by reducing neutrophil accumulation in reperfused ischaemic myocardium, 31 dogs underwent a 2 h occlusion of the left anterior descending coronary artery, followed by 6 h of reperfusion. One group of dogs received saline (controls) the other a perfusion of lignocaine 0.06 mg·kg−1·min−1 starting 30 min before coronary occlusion and lasting for the duration of the experiment. Blood lignocaine concentrations at the onset of reperfusion were 3.3(0.6) μg·ml−1. 111Indium labelled autologous neutrophils were injected at the time of occlusion and their accumulation in the myocardium measured by digital scintigraphy of heart slices. The area at risk and infarct size were evaluated by planimetry of the heart slices (7 mm) after perfusion of Evans blue dye and triphenyltetrazolium staining. Ventricular fibrillation occurred in six controls and in five dogs receiving lignocaine. The phenomenon occurred early during the occlusion period in the lignocaine group (five dogs) and at reperfusion in controls (five dogs; p
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/22.6.439