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La estimulación vagal eferente preisquémica aumenta el tama?o del infarto de miocardio en conejosKeywords: myocardial infarction, vagal stimulation, atropine, esmolol, atenolol. Abstract: it has been shown that vagal stimulation induces cardioprotective effects and the administration of acetylcholine mimics ischemic preconditioning. however, there are no conclusive data about the effects of in vivo vagal stimulation on myocardial infarction. the objective of this study was to evaluate the effects of vagal stimulation on experimental myocardial infarction induced in rabbits subjected to 45 min of regional myocardial ischemia by ligation of a branch of the left coronary artery, followed by 4 hours of reperfusion (g1, n=14). in group 2 (g2, n=9) g1 protocol was repeated and, before inducing ischemia, right efferent vagal stimulation was performed during 10 min to an intensity enough to reduce heart rate by 10-20% followed by a recovery period of 5 min. in group 3 (g3, n=5) the g2 protocol was repeated, but atropine was administered during vagal stimulation. in other experimental groups the g2 protocol was repeated and short-acting β1 -adrenergic blocker (esmolol, g4, n=7) or long-acting beta blocker (atenolol, g5, n=5) were administered during the stimulation. preischemic vagal stimulation increased the infarct size from 45.2%±2.4% to 62.9%±3.1% (p <0.05). atropine reverted this effect reducing the infarct size to 44.8%±3.9% (p <0.05 vs. g2). the administration of esmolol or atenolol attenuated the increase in infarct size to 50.1%±4.2% and 50.0%±2.9%, respectively (p <0,05). preischemic efferent vagal stimulation significantly increases the infarct size by a muscarinic cholinergic mechanism. this effect is reverted by beta adrenergic blockade. applying vagal stimulation to different clinical scenarios might cause deleterious secondary effects.
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