Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 500-507 |
| Number of pages | 8 |
| Journal | Journal of Cardiovascular Pharmacology |
| Volume | 58 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Nov 2011 |
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Keywords
- autonomic nervous system
- infarct size
- inflammatory markers
- ischemia/reperfusion
- myocardial infarction
- vagal activity
ASJC Scopus subject areas
- Pharmacology
- Cardiology and Cardiovascular Medicine
Cite this
Vagal stimulation, through its nicotinic action, limits infarct size and the inflammatory response to myocardial Ischemia and reperfusion. / Calvillo, Laura; Vanoli, Emilio; Andreoli, Elisa; Besana, Alessandra; Omodeo, Elisabetta; Gnecchi, Massimiliano; Zerbi, Pietro; Vago, Gianluca; Busca, Giuseppe; Schwartz, Peter J.
In: Journal of Cardiovascular Pharmacology, Vol. 58, No. 5, 11.2011, p. 500-507.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Vagal stimulation, through its nicotinic action, limits infarct size and the inflammatory response to myocardial Ischemia and reperfusion
AU - Calvillo, Laura
AU - Vanoli, Emilio
AU - Andreoli, Elisa
AU - Besana, Alessandra
AU - Omodeo, Elisabetta
AU - Gnecchi, Massimiliano
AU - Zerbi, Pietro
AU - Vago, Gianluca
AU - Busca, Giuseppe
AU - Schwartz, Peter J.
PY - 2011/11
Y1 - 2011/11
N2 - 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.
AB - 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.
KW - autonomic nervous system
KW - infarct size
KW - inflammatory markers
KW - ischemia/reperfusion
KW - myocardial infarction
KW - vagal activity
UR - http://www.scopus.com/inward/record.url?scp=80955144444&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80955144444&partnerID=8YFLogxK
U2 - 10.1097/FJC.0b013e31822b7204
DO - 10.1097/FJC.0b013e31822b7204
M3 - Article
C2 - 21765369
AN - SCOPUS:80955144444
VL - 58
SP - 500
EP - 507
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 5
ER -