• The Korean Journal of Physiology and Pharmacology
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• 제18권5호
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• pp.411-418
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• 2014

Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group ($ED_{50}=1.44{\times}10^5M$ vs. $4.9{\times}10^6M$) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group ($ED_{50}=6.17{\times}10^7M$ vs. $2.82{\times}10^7M$) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2001년도 추계학술대회논문집B
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• pp.529-532
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• 2001

The purposes of the present study are to investigate hemodynamic characteristics and to define shear-sensitive remodeling in the stenosed coronary models. Two models for the compensatory remodelling used for this research are a pre-stenotic dilation and a post-stenotic dilation models for the computer simulation. The peak wall shear stress on the post-stenotic model is higher than that of the pre-stenotic model. Two recirculation zones are generated in the pre-stenotic model, and the zones in the pre-stenotic model are smaller than those in the post-stenotic model. Variation of the wall shear stress in the pre-stenotic model is lower than that in the post-stenotic model. In computer simulation with the post-stenotic model, higher temporal and spatial shear fluctuation and stress suggested shear-sensitive remodeling. Shear-sensitive remodeling may be associated with the increased risk of plaque rupture, the underlying cause of acute coronary syndromes, and sudden cardiac death.