Vagal Stimulation, Through its Nicotinic Action, Limits Infarct Size and the Inflammatory Response to Myocardial Ischemia and Reperfusion
| Autor: | Elisabetta Omodeo, Alessandra Besana, Emilio Vanoli, Laura Calvillo, Peter J. Schwartz, Giuseppe Busca, Elisa Andreoli, Pietro Zerbi, Massimiliano Gnecchi, Gianluca Vago |
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| Rok vydání: | 2011 |
| Předmět: |
Male
Chemokine CXCL5 medicine.medical_specialty Vagus Nerve Stimulation alpha7 Nicotinic Acetylcholine Receptor Neutrophils medicine.medical_treatment Myocardial Infarction Ischemia Apoptosis Myocardial Reperfusion Injury Inflammation Nicotinic Antagonists Mecamylamine Receptors Nicotinic Rats Sprague-Dawley Heart Rate Internal medicine Heart rate medicine Animals Myocardial infarction Chemokine CCL2 Pharmacology business.industry Macrophages Myocardium Cardiac Pacing Artificial medicine.disease Rats Autonomic nervous system Heart failure Cardiology medicine.symptom Cardiology and Cardiovascular Medicine business Vagus nerve stimulation medicine.drug |
| Zdroj: | Journal of Cardiovascular Pharmacology. 58:500-507 |
| ISSN: | 0160-2446 |
| DOI: | 10.1097/fjc.0b013e31822b7204 |
| Popis: | Vagal activity has protective effects in ischemic heart disease. We tested whether vagal stimulation (VS) could modulate the inflammatory reaction, a major determinant of cardiac injury after ischemia/reperfusion. Four groups of male rats underwent myocardial ischemia (30 minutes) and reperfusion (24 hours). One group underwent VS (40 minutes), 1 VS plus atrial pacing (VS + Pacing), and 1 VS plus nicotinic inhibition by mecamylamine (VS + MEC). After 24 hours, the area at risk, infarct size, inflammation parameters, and apoptosis were quantified. Infarct size was reduced in all VS-treated rats (controls, 53 ± 18%; VS, 6.5 ± 3%; VS + Pacing, 23 ± 6%; VS + MEC, 33 ± 9%; P < 0.005 vs. controls). The infarct size in the VS + MEC group was larger than that in VS-treated animals, despite similar heart rate, suggesting partial loss of protection. The number of macrophages, neutrophils, and apoptotic cells in the area at risk and the plasma cytokines levels were significantly reduced in all VS-treated animals. In conclusion, VS decreases infarct size and inflammatory markers during ischemia/reperfusion independent of the heart rate. The anti-inflammatory and antiapoptotic properties of the nicotinic pathway are the primary underlying mechanism. The vagally mediated modulation of inflammatory responses may prove valuable in the clinical management of acute coronary syndromes and of heart failure. |
| Databáze: | OpenAIRE |
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