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

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Abstract
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; p111In labelled neutrophil and circulating neutrophil counts at the onset of reperfusion (r=0.076, p111In neutrophil counts per cm2 of tissue were statistically similar in controls (9725(1669)) and lignocaine treated dogs (11631(3317)). Infarct size expressed as a percentage of the area at risk was also similar in both groups (controls 36.1(7.1)%; lignocaine 35.8(6.3)%). Thus lignocaine does not reduce infarct size and myocardial neutrophil accumulation after a 2 h coronary occlusion in the dog. Furthermore, these results suggest that lignocaine may induce ventricular fibrillation during coronary occlusion.

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