INHALED CIGARETTE SMOKE ACCELERATES VOLUME OVERLOAD INDUCED CARDIAC INJURY
Document Type
Presentation
Start Date
22-10-2010 3:00 PM
End Date
22-10-2010 4:30 PM
Description
In patients with heart failure, cigarette smoking is linked to sudden cardiac death and accelerated decompensation. Cigarette smoke exposure causes activation of inflammatory and oxidative stress pathways. In this study, we examine the effects of cigarette smoke inhalation on the stressed heart. Our hypothesis is that cigarette smoke exacerbates cardiac injury by accelerating ventricular remodeling and dysfunction. Volume overload (VO) stress was surgically induced in rats by an abdominal AV shunt. This stress produces a pattern of myocardial remodeling similar to clinical presentations of heart failure. Male rats, with and without VO, were exposed to either room air or cigarette smoke (6 cig/day) for six weeks. Echocardiogram measurements taken at baseline and weekly thereafter provided functional assessment of LV internal dimension (ID), wall thickness, and ejection fraction (EF). Collagen volume fraction of mid-ventricular regions was measured using Picrosirius Red staining. VO animals exposed to cigarette smoke had significantly increased LVID (10.5 ± 0.2 vs 9.6 ± 0.2 mm), decreased posterior wall thickness (0.82 ± 0.04 vs 0.98 ± 0.05 mm), and reduced EF (63 ± 2 vs 68 ± 2 %) compared to VO rats exposed to room air. The morphological analysis of ventricular collagen revealed that the VO animals exposed to cigarette smoke had significantly decreased collagen compared to those exposed to room air (0.92 ± 0.11 vs 1.63 ± 0.17 %total LV area). Western blot analysis of MMP-2 expression indicated a significant increase in the ratio of active to inactive forms in the VO animals exposed to cigarette smoke compared to all other groups. These data indicate that cigarette smoke inhalation worsens VO-induced cardiac injury and accelerates interstitial collagen loss, ventricular wall thinning, dilatation and dysfunction.
Recommended Citation
Bradley, Jessica and Gardner, J. D., "INHALED CIGARETTE SMOKE ACCELERATES VOLUME OVERLOAD INDUCED CARDIAC INJURY" (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 3.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/poster2/3
INHALED CIGARETTE SMOKE ACCELERATES VOLUME OVERLOAD INDUCED CARDIAC INJURY
In patients with heart failure, cigarette smoking is linked to sudden cardiac death and accelerated decompensation. Cigarette smoke exposure causes activation of inflammatory and oxidative stress pathways. In this study, we examine the effects of cigarette smoke inhalation on the stressed heart. Our hypothesis is that cigarette smoke exacerbates cardiac injury by accelerating ventricular remodeling and dysfunction. Volume overload (VO) stress was surgically induced in rats by an abdominal AV shunt. This stress produces a pattern of myocardial remodeling similar to clinical presentations of heart failure. Male rats, with and without VO, were exposed to either room air or cigarette smoke (6 cig/day) for six weeks. Echocardiogram measurements taken at baseline and weekly thereafter provided functional assessment of LV internal dimension (ID), wall thickness, and ejection fraction (EF). Collagen volume fraction of mid-ventricular regions was measured using Picrosirius Red staining. VO animals exposed to cigarette smoke had significantly increased LVID (10.5 ± 0.2 vs 9.6 ± 0.2 mm), decreased posterior wall thickness (0.82 ± 0.04 vs 0.98 ± 0.05 mm), and reduced EF (63 ± 2 vs 68 ± 2 %) compared to VO rats exposed to room air. The morphological analysis of ventricular collagen revealed that the VO animals exposed to cigarette smoke had significantly decreased collagen compared to those exposed to room air (0.92 ± 0.11 vs 1.63 ± 0.17 %total LV area). Western blot analysis of MMP-2 expression indicated a significant increase in the ratio of active to inactive forms in the VO animals exposed to cigarette smoke compared to all other groups. These data indicate that cigarette smoke inhalation worsens VO-induced cardiac injury and accelerates interstitial collagen loss, ventricular wall thinning, dilatation and dysfunction.
Comments
See abstract book page 47