Effects of transdermal nicotine treatment on structure and function of coronary artery bypass grafts

Clouse, W. Darrin; Yamaguchi, Hiroki; Phillips, Michael; Hurt, R. Douglas; Fitzpatrick, Lorraine A.; Moyer, Thomas P.; Rowland, Charles; Schaff, Hartzell V.; Miller, Virginia M.

doi:10.1152/jappl.2000.89.3.1213

Cited by 20 publications

(7 citation statements)

References 40 publications

(53 reference statements)

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“…Although nicotine plays a major role in smoking-related increases in cardiac output, heart rate, and blood pressure, its role in CS-related athero-thrombotic disease remains controversial (17,84 -89). Nicotine exposure alone had been reported to cause no change, a decrease, or an increase in EDV or NO availability (85)(86)(87)(88). In various models, although high doses of nicotine favor atherogenic changes, the majority of current evidence suggests that nicotine, at concentrations similar to a smoker's blood level, has a minor effect on the initiation or propagation of atherosclerosis (17,85).…”

Section: Factors and Mechanisms Responsible For Smoking-mediated Vascmentioning

confidence: 99%

The pathophysiology of cigarette smoking and cardiovascular disease

Ambrose¹,

Barua²

2004

Journal of the American College of Cardiology

1,907

1,411

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Cigarette smoking (CS) continues to be a major health hazard, and it contributes significantly to cardiovascular morbidity and mortality. Cigarette smoking impacts all phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive (environmental) cigarette smoke exposure predispose to cardiovascular events. Whether there is a distinct direct dose-dependent correlation between cigarette smoke exposure and risk is debatable, as some recent experimental clinical studies have shown a non-linear relation to cigarette smoke exposure. The exact toxic components of cigarette smoke and the mechanisms involved in CS-related cardiovascular dysfunction are largely unknown, but CS increases inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction.

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Section: Factors and Mechanisms Responsible For Smoking-mediated Vascmentioning

confidence: 99%

The pathophysiology of cigarette smoking and cardiovascular disease

Ambrose¹,

Barua²

2004

Journal of the American College of Cardiology

1,907

1,411

View full text Add to dashboard Cite

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“…Although many nicotine-induced pathophysiological changes in the cardiovascular system have been determined, the specific mechanisms through which these pathologies occur have not been completely elucidated. In some cases, the effects of nicotine on a particular component of the cardiovascular physiology are controversial (Li et al, 1994;Clouse et al, 2000).…”

mentioning

confidence: 99%

Fetal and Neonatal Nicotine Exposure Differentially Regulates Vascular Contractility in Adult Male and Female Offspring

Xiao¹,

Huang²,

Lawrence³

et al. 2006

J Pharmacol Exp Ther

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Epidemiologic studies suggest that prenatal exposure to maternal cigarette smoking is associated with an increased risk of elevated blood pressure in postnatal life. The present study was designed to test the hypothesis that fetal and neonatal nicotine exposure increased vascular contractility in adult offspring. Nicotine was administered to pregnant rats via s.c. osmotic minipumps throughout gestation and up to 10 days after delivery. Aortas were isolated from adult male and female offspring at the age of 3 months old. Nicotine significantly increased KCland norepinephrine-induced contractions of the aorta in male, but not female, offspring. Inhibition of endothelial nitric oxide synthase (eNOS) with N G -nitro-L-arginine (L-NNA) significantly increased norepinephrine-induced contractions in control male offspring but showed no effect in nicotine-treated male offspring. In the presence of L-NNA, there was no significant difference in norepinephrine-induced contractions between control and nicotine-treated males. In contrast, nicotine caused a significant increase in L-NNA-mediated potentiation of norepinephrine-induced contractions in female offspring. Nicotine had no effect on sodium nitroprusside-induced endotheliumindependent relaxations of aortas from either male or female offspring. However, it decreased endothelium-dependent relaxations induced by acetylcholine in male offspring but increased them in females. There were no differences in eNOS protein levels in aortas between the control and nicotinetreated animals in either male or female offspring. The results suggest that fetal and neonatal nicotine exposure alters vascular functions in adult offspring in a gender-specific manner, which may lead to an increased risk of cardiovascular dysfunction in later life.

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“…BSP binds collagen and is associated with the early phases of bone formation, acting as a potent and specific nucleator of hydroxylapatite (20,28). BSP is expressed in vein grafts and aortic valves prior to demonstration of overt calcification (13,44).…”

mentioning

confidence: 99%

Differential effects of 17β-estradiol and raloxifene on VSMC phenotype and expression of osteoblast-associated proteins

Rzewuska-Lech¹,

Jayachandran²,

Fitzpatrick³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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Rzewuska-Lech, Ewa, Muthuvel Jayachandran, Lorraine A. Fitzpatrick, and Virginia M. Miller. Differential effects of 17␤-estradiol and raloxifene on VSMC phenotype and expression of osteoblast-associated proteins. Am J Physiol Endocrinol Metab 289: E105-E112, 2005. First published February 15, 2005 doi:10.1152/ajpendo.00366.2004.-Several studies demonstrate an association between osteoporosis and arterial calcific disease, both of which being common in elderly women. Estradiol and raloxifene, a selective estrogen receptor modulator, prevent bone loss in postmenopausal women. Little is known regarding how these agents affect arterial calcification. The aim of this study was to determine whether or not 17␤-estradiol and raloxifene reduced vascular smooth muscle cell (VSMC) differentiation and expression of bone-associated proteins during phosphate-induced calcification in vitro. Aortic VSMC were cultured from adult, gonadally intact, and ovariectomized (OVX) female pigs. Calcifying medium was added, and cells were treated with solvent (control), 17␤-estradiol (E2), or raloxifene. Extent of calcification and phenotypic expression of bone-associated proteins [matrix gla protein (MGP), osteoprotegerin (OPG), and bone sialoprotein (BSP)] were examined at 3-day intervals over 2 wk. Calcium content increased in all groups but was greater in VSMC derived from intact compared with OVX animals. E 2 reduced calcification and preserved a contractile phenotype. Expression of OPG significantly decreased with time; this decrease was significantly greater in VSMC derived from OVX compared with gonadally intact pigs. E 2 and raloxifene preserved expression of OPG only in VSMC from intact pigs. Expression of MGP increased significantly with time and was not affected by E 2 or raloxifene treatments. E2 treatment significantly inhibited synthesis of BSP in cells from both groups. In conclusion, E2 slows differentiation of VSMC induced by excess phosphate. Effectiveness of raloxifene to preserve expression of bone cell-associated proteins depends on the hormonal status of the tissue donor. vascular smooth muscle cells; estrogen; raloxifene; selective receptor modulator; smooth muscle phenotype

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Effects of transdermal nicotine treatment on structure and function of coronary artery bypass grafts

Cited by 20 publications

References 40 publications

The pathophysiology of cigarette smoking and cardiovascular disease

The pathophysiology of cigarette smoking and cardiovascular disease

Fetal and Neonatal Nicotine Exposure Differentially Regulates Vascular Contractility in Adult Male and Female Offspring

Differential effects of 17β-estradiol and raloxifene on VSMC phenotype and expression of osteoblast-associated proteins

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