Document Detail


Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice.
MedLine Citation:
PMID:  21057039     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cigarette smoking is a major independent risk factor for cardiovascular disease. While the association between chronic smoking and cardiovascular disease is well established, the underlying mechanisms are incompletely understood, partly due to the lack of adequate in vivo animal models. Here, we report a mouse model of chronic smoking-induced cardiovascular pathology. Male C57BL/6J mice were exposed to whole body mainstream cigarette smoke (CS) using a SCIREQ "InExpose" smoking system (48 min/day, 5 days/wk) for 16 or 32 wk. Age-matched, air-exposed mice served as nonsmoking controls. Blood pressure was measured, and cardiac MRI was performed. In vitro vascular ring and isolated heart experiments were performed to measure vascular reactivity and cardiac function. Blood from control and smoking mice was studied for the nitric oxide (NO) decay rate and reactive oxygen species (ROS) generation. With 32 wk of CS exposure, mice had significantly less body weight gain and markedly higher blood pressure. At 32 wk of CS exposure, ACh-induced vasorelaxation was significantly shifted to the right and downward, left ventricular mass was significantly larger along with an increased heart-to-body weight ratio, in vitro cardiac function tended to be impaired with high afterload, white blood cells had significantly higher ROS generation, and the blood NO decay rate was significantly faster. Thus, smoking led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability, and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease. This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases.
Authors:
M A Hassan Talukder; Wesley M Johnson; Saradhadevi Varadharaj; Jiarui Lian; Patrick N Kearns; Mohamed A El-Mahdy; Xiaoping Liu; Jay L Zweier
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-11-05
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  300     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-04     Completed Date:  2011-01-28     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H388-96     Citation Subset:  IM    
Affiliation:
Center for Environmental and Smoking-Induced Diseases, Davis Heart and Lung Research Institute, and Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Blood Pressure
Body Weight
Endothelium, Vascular / metabolism,  physiopathology*
Heart / physiopathology
Hypertension / etiology*,  metabolism
Magnetic Resonance Imaging
Male
Mice
Myocardium / metabolism
Nitric Oxide / metabolism*
Oxidative Stress*
Reactive Oxygen Species / metabolism
Risk Factors
Smoke
Smoking / adverse effects*
Tobacco
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
EB-0890/EB/NIBIB NIH HHS; EB-4900/EB/NIBIB NIH HHS; HL-38324/HL/NHLBI NIH HHS; HL-63744/HL/NHLBI NIH HHS; HL-65608/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 0/Smoke; 10102-43-9/Nitric Oxide
Comments/Corrections

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