Document Detail

Antioxidant N-acetyl cysteine reverses cigarette smoke-induced myocardial infarction by inhibiting inflammation and oxidative stress in a rat model.
MedLine Citation:
PMID:  21968809     Owner:  NLM     Status:  Publisher    
The contribution of chronic tobacco exposure in determining post-myocardial infarction (MI) left ventricular (LV) remodeling and possible therapeutic strategies has not been investigated systematically. In this small animal investigation, we demonstrate that chronic tobacco smoke exposure leading up to acute MI in rats is associated with greater histological extent of myocardial necrosis and consequent worse LV function. These findings are associated with increased transcriptomic expression of pro-inflammatory cytokines, tissue repair molecules and markers of oxidative stress in the myocardium. The results demonstrate that an N-acetyl cysteine (NAC) treatment significantly reduced tobacco-exposed induced infarct size and percent fractional shortening. A significantly increased LV end-systolic diameter was observed in tobacco-exposed sham compared to tobacco-naïve sham (4.92±0.41 vs 3.45±0.33; P<0.05), and tobacco-exposed MI compared to tobacco-naïve MI (8.24±0.3 vs 6.1±0.49; P<0.01) rats. Decreased intracardiac mRNA expression of the markers of inflammation, tissue repair and oxidative stress and circulating levels of pro-inflammatory cytokines accompanied these positive effects of NAC. The treatment of tobacco-exposed MI rats with NAC resulted in significantly increased levels of intracardiac mRNA expression of antioxidants, including superoxide dismutase, thioredoxin and nuclear factor-E2-related factor 2, as well as circulating levels of glutathione (7±0.12 vs 10±0.18; P0.001), where the levels were almost identical to the tobacco-naïve sham rats. These findings identify a novel post-infarction therapy for amelioration of the adverse effects of tobacco exposure on the infracted myocardium and advocate the use of dietary supplement antioxidants for habitual smokers to prevent and reverse cardiovascular adverse effects in the absence of successful achievement of cessation of smoking.Laboratory Investigation advance online publication, 3 October 2011; doi:10.1038/labinvest.2011.146.
Ashwani K Khanna; Jianping Xu; Mandeep R Mehra
Related Documents :
3425559 - An animal model to examine the response to environmental stress as a factor in sudden c...
24485519 - 2013 update on congenital heart disease, clinical cardiology, heart failure, and heart ...
12668859 - Inflammation, platelets, and glycoprotein iib/iiia inhibitors.
20608989 - Role of drugs and devices in patients at risk of sudden cardiac death.
20129539 - Will imaging assist in the selection of patients with heart failure for an icd?
22327939 - Correlation of left ventricular wall thickness, heart mass, serological parameters and ...
9313019 - Functional recovery after myocardial infarction in men: the independent effects of soci...
18929239 - The ciao (coronary interventions antiplatelet-based only) study: a randomized study com...
10469959 - Release of cardiac troponin i in antegrade crystalloid versus cold blood cardioplegia.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-10-03
Journal Detail:
Title:  Laboratory investigation; a journal of technical methods and pathology     Volume:  -     ISSN:  1530-0307     ISO Abbreviation:  -     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-4     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376617     Medline TA:  Lab Invest     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
1] Department of Pathology, University of Maryland, Baltimore, MD, USA [2] OncoDetect, Baltimore, MD, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Prospective analysis of KRAS wild-type patients with metastatic colorectal cancer using cetuximab pl...
Next Document:  Roles of ?-catenin signaling in phenotypic expression and proliferation of articular cartilage super...