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Nicotine Reduced Post‐Infarct Inflammation and Improved Cardiac Output during Exercise in Conscious Mice
Author(s) -
Lujan Heidi L.,
Wang Richard,
Blumberg Amanda J.,
DiCarlo Stephen E.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1128.17
Subject(s) - nicotine , medicine , inflammation , nicotinic agonist , cholinergic , cardiac function curve , acetylcholine , myocardial infarction , cardiology , ischemia , endocrinology , receptor , heart failure
Myocardial ischemia/reperfusion and infarction (I/R/I) have complex and lethal effects on the myocardium due, in part, to the inflammatory and reparative processes. Although inflammatory mediators are essential, an excessive inflammatory response extends the injury. Thus, there is a critically fine balance between the beneficial effects of the inflammatory response and the potential of extending the myocardial injury. The management of this balance should center on endogenous modulators of the inflammatory and reparative processes because physiological mechanisms may be the most effective and innocuous strategy. Accordingly, activation of the Cholinergic Anti‐Inflammatory Pathway (CAP) was hypothesized to be an important strategy. The CAP is an endogenous mechanism by which acetylcholine, via the α7 subunit of the nicotinic acetylcholine receptor, interacts with the innate immune system to modulate and restrain the inflammatory cascade. Thus, we hypothesized that application of the nicotine patch would reduce post‐infarct macrophage infiltration and improve cardiac function during exercise in conscious mice. We implanted a Doppler ultra‐sonic flow probe on the ascending aorta and coronary artery occluder for repeated measurements of cardiac output in conscious mice, at rest and during exercise, before and during I/R/I. The nicotine patch attenuated post‐infarct leukocyte recruitment (1005 ± 296 versus 3210 ± 460 cells/mm 2 ), reduced infarct size (66 ± 6 versus 38 ± 11 %), and improved maximum cardiac output during exercise (13.2 ± 1.2 versus 16.4 ± 1.6 ml/min) following I/R/I in conscious mice.