Cigarette smoking increases the development of intimal hyperplasia after vascular injury

Law, Michael M.; Gelabert, Hugh A.; Moore, Wesley S.; Hajjar, George E.; Colburn, Michael D.; Petrik, Pavel V.; Quiñones-Baldrich, William J.

doi:10.1016/s0741-5214(96)80004-8

Cited by 26 publications

(18 citation statements)

References 36 publications

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“…CS exposure in WT mice was associated with increased arterial iNOS expression, superoxide production, activator protein-1 (AP-1) activation, and serum NO. 4,5 In the Atherosclerosis Risk in Communities Study, active smoking and exposure to environmental tobacco smoke were associated with accelerated progression of intimal/medial thickness of the carotid artery. 6 The underlying mechanism(s) of these deleterious effects remain unknown.…”

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confidence: 99%

Effect of Exposure to Cigarette Smoke on Carotid Artery Intimal Thickening

Anazawa

Dimayuga

et al. 2004

ATVB

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Objective-We investigated the role of inducible NO synthase (iNOS) in intimal thickening with exposure to cigarette smoke (CS). Methods and Results-Intimal thickening in wild-type (WT) and iNOS-deficient (iNOSϪ/Ϫ) mice subjected to CS exposure was induced by placement of a cuff around the carotid artery. CS exposure in WT mice was associated with increased arterial iNOS expression, superoxide production, activator protein-1 (AP-1) activation, and serum NO. 4,5 In the Atherosclerosis Risk in Communities Study, active smoking and exposure to environmental tobacco smoke were associated with accelerated progression of intimal/medial thickness of the carotid artery. 6 The underlying mechanism(s) of these deleterious effects remain unknown. 7,8 Increased transcription factor activation, expression of adhesion molecules, and redox gene inducible NO synthase (iNOS) have been demonstrated with exposure to cigarette smoke (CS) 9 -11 and may contribute to increased intimal thickening.The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor mediating enzyme induction in response to CS and may have a potentiating effect on CS carcinogenicity. 12 The mouse iNOS promoter 13 contains a site that corresponds to the core xenobiotic-responsive element (XRE) to which the AhR binds. Therefore, the AhR may mediate the negative effects of CS on the arterial intima.We hypothesized that exposure to CS increases iNOS gene expression and activity in the arterial wall leading to augmented intimal thickening after injury. We used a model of intimal thickening induced by placement of a periadventitial cuff around the right carotid artery of mice exposed to CS. Cultured aortic smooth muscle cells (SMCs) were used to investigate the AhR pathway for increased iNOS expression after exposure to CS condensate (CSC). Materials and Methods AnimalsMale wild-type (WT) and iNOS-deficient (iNOSϪ/Ϫ) mice with the C57BL/6J background strain (The Jackson Laboratory) were fed normal chow throughout the study period. At the age of 25 weeks, mice were anesthetized with Avertin (0.016 mL/g of 2.5% solution IP), and the right carotid artery was carefully isolated under a dissecting microscope. A nonocclusive plastic cuff was placed around the right carotid artery, and the skin incision was closed, as described previously. 14 Mice were euthanized 3, 7, or 21 days after cuff placement. The carotid arteries were perfused with 0.9% saline

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confidence: 99%

Effect of Exposure to Cigarette Smoke on Carotid Artery Intimal Thickening

Anazawa

Dimayuga

et al. 2004

ATVB

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“…Our previous studies in the rat carotid artery demonstrated an increase in neointimal hyperplasia in this deendothelialized model [9,23]. Thus in two distinct models of arterial injury, this method of cigarette smoke exposure causes an increase in smooth muscle growth as well as endothelial regrowth.…”

Section: Figmentioning

confidence: 59%

Effect of Cigarette Smoke on Endothelial Regenerationin Vivoand Nitric Oxide Levels

Sarkar

Gelabert

Mohiuddin

et al. 1999

Journal of Surgical Research

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“…This is caused by invasion and proliferation of smooth muscle cells, fibroblasts and matrix material derived from the cut end of the host artery. It has been reported that the risk factors for the genesis and development of atherosclerosis, such as smoking, diabetes, harvesting and preparation of the vein grafts, are important factors [9,10].…”

Section: Discussionmentioning

confidence: 99%

“…Although the factors that lead to myointimal hyperplasia in arterial vein grafts are unknown, growth factors like platelet-derived growth factor are powerful mitogens for smooth muscle cells that have been implicated in the genesis of myointimal hyperplasia [2,9,[12][13][14]. Sterpetti et al [2] observed in a rat model that myointimal hyperplasia formation and regression in experimental vein grafts correlate with growth factor production.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

Işcan

Saritaş

et al. 1998

Eur Surg Res

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Purpose: The aim of this study was to evaluate the efficacy of octreotide in modulating the progression of intimal hyperplasia in autogenous vein bypass grafts in a canine model. The effect of the drug on the progression of intimal hyperplasia was measured with the Gilman parameter, a measure used extensively as a wound-healing descriptor. Methods: 12 mongrel dogs were randomly and equally divided into two groups. The first group (octreotide group) was administered octreotide 20 µg/kg/day. The control group (group II) received saline solution by subcutaneous injection. Each dog had 8- to 10-cm segments of autogenous jugular vein bypassed to the femoral arteries. Quantitative data on luminel narrowing over time from intimal hyperplasia were compared from calculated Gilman parameters after image analysis of retrieved, histologically processed graft sections. Each vein graft was analyzed by computerized morphometric analysis. Results: The mean Gilman parameter for distal graft segments was 0.47 ± 0.17 mm in the control group and 0.25 ± 0.07 mm in the octreotide group 6 weeks after operation (p < 0.05). Distal graft segments between the control and octreotide groups were statistically significant. In proximal, medial and distal graft segments, the mean Gilman parameters were 0.51 ± 0.16 mm in the control group and 0.37 ± 0.18 mm in the octreotide group, the difference being statistically significant (p < 0.01). Conclusion: Octreotide significantly inhibits myointimal thickening, and these data support the efficacy of octreotide in reducing intimal hyperplasia in arterialized vein grafts during the short postoperative period. Further investigations are required to as certain whether this beneficial effect of octretide persists in the long term.

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Cigarette smoking increases the development of intimal hyperplasia after vascular injury

Abstract: Inhalation of cigarette smoke increases the development of intimal hyperplasia in a rat model of a balloon catheter arterial injury.

Cited by 26 publications

References 36 publications

Effect of Exposure to Cigarette Smoke on Carotid Artery Intimal Thickening

Effect of Exposure to Cigarette Smoke on Carotid Artery Intimal Thickening

Effect of Cigarette Smoke on Endothelial Regenerationin Vivoand Nitric Oxide Levels

Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

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