Experimental model to study the effect of nicotine in a random skin flap, in the rat

Gomes, Heitor Carvalho; Campos, José Humberto Oliveira; Ferreira, Lydia Masako; Kobayashi, Ludmila

doi:10.1590/s0102-86502004000700012

Cited by 8 publications

(8 citation statements)

References 10 publications

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“…The study subjects were 16 9 and injected in the subcutaneous tissues of the rats from groups 1 and 2, daily, one week before and one week after surgery, with a dose of 2mg/Kg. This study was approved by the Committee of Ethics in Animal Experiments of FMRP-USP, protocol no.…”

Section: Experimentation Animalsmentioning

confidence: 99%

“…5 Surveys using low intensity laser have appeared recently. 7 In several experimental studies, various authors 8,9 investigated the cause and the deleterious effect of cigarette smoke or of nicotine separately. These studies, using different methodologies as regards the number and species of animals, type and time of exposure (smoke or nicotine), dosage of nicotine or of smoke, and type of surgery, observed a deleterious effect in the skin flaps exerted both by nicotine alone, and by cigarette smoke, causing an increase of the area of necrosis in the flap.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 According to Prado et al 7 , low intensity laser therapy has been used to decrease the skin flap necrosis area in rats, as it is said to cause an increase in microcirculation and in vascular neoformation, favoring ischemic flaps. Due to the shortage of studies using laser therapy to minimize the deleterious effects of nicotine, this study was carried out with low intensity laser therapy in an attempt to block these effects, bringing about an increase in the viability of the random skin flap in rats.…”

Section: Introductionmentioning

confidence: 99%

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Laser 830nm na viabilidade do retalho cutâneo de ratos submetidos à nicotina

et al. 2011

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Objective: To investigate the possible effects of laser diode 830nm counter to the action of nicotine on the viability of the skin flap in rats. Methods: 24 Wistar-albino rats were used, divided into 3 groups of 8: Group 1 -subject to the surgical technique to obtain the random skin flap in cranial base, subcutaneous injection of nicotine of 2mg/Kg/day a week before and one week after surgery and simulation of laser. Group 2 -similar to group 1, the random skin flap in the cranial base were subjected to laser irradiation immediately after surgery and on the subsequent 4 days. After euthanasia, areas of necrosis and viable tissue were examined by a manual method (weighing the Role of Feedback) and by the semi-automated method of analysis (Mini-Mop ® ). Results: The results were statistically analyzed by ANOVA. The values of the percentage of necrotic area by the method of analysis showed a decreased area of necrosis in group 2 where the laser was applied. Conclusion: The 830nm laser was effective in improving the viability of skin flaps in rats subjected to the action of nicotine. Level of evidence II: Therapeutic Studies -Investigating the results of treatment.

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Section: Experimentation Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Laser 830nm na viabilidade do retalho cutâneo de ratos submetidos à nicotina

et al. 2011

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“…, that allows plasma levels similar to those found in the light smoker (Gomes et al, 2004). The dose of nicotine used and the duration of nicotine exposure was previously confirmed to show induction of oxidative stress and tissue damage (Helen et al, 2003).…”

Section: Analysis Of Mpomentioning

confidence: 61%

The effects of erdosteine, N‐acetylcysteine and vitamin E on nicotine‐induced apoptosis of cardiac cells

Demiralay

Gürsan

Erdem

2007

J of Applied Toxicology

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This study was conducted to investigate the frequency of apoptosis in rat cardiomyocytes after intratraperitoneal nicotine injection, in order to examine the roles of inflammatory markers [myeloperoxidase (MPO) and tumor necrosis factor alpha (TNF-alpha)] in nicotine-induced cardiac damage and to determine the protective effects of three known antioxidant agents (N-acetylcysteine (NAC), erdosteine and vitamin E) on nicotine toxicity in the heart. Female Wistar rats were divided into seven groups, each composed of nine rats: two negative control groups, two positive control groups, one erdosteine-treated group (500 mg kg(-1)), one NAC-treated group (500 mg kg(-1)) and one vitamin E-treated group (500 mg kg(-1)). Nicotine was intraperitoneally injected at a dosage of 0.6 mg kg(-1) for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Heart tissue samples were stained with hematoxylin-eosin for histopathological assessments. Apoptosis level in cardiomyocytes was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Staining of cytoplasmic TNF-alpha in cardiomyocytes and heart MPO activity were evaluated by immunohistochemistry. The treatments with erdosteine, NAC and vitamin E significantly reduced the rate of nicotine-induced cardiomyocyte apoptosis. The effect of vitamin E on apoptosis regulation was weaker than the effects of erdosteine and NAC. Erdosteine, NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and heart MPO activity. This findings suggest that the effects of erdosteine and NAC on apoptosis regulation are stronger than that of vitamin E.

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“…As regards via of administration and dose of nicotine, the intraperitoneal injection, is the choice, in a dose of 0.6 mg/kg/day, that allows plasmatic levels similar to those found in the light smoker. 23 Dose of nicotine used and duration of nicotine exposure was previously confirmed to show induction of oxidative stress and tissue damage. 16 NAC and vitamin E significantly reduced endothelial damage, subendothelial disruption, and subendothelial edema.…”

Section: Discussionmentioning

confidence: 94%

Regulation of nicotine-induced apoptosis of pulmonary artery endothelial cells by treatment of N-acetylcysteine and vitamin E

2007

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This study investigated the frequency of apoptosis in rat pulmonary artery endothelial cells after intraperitoneal nicotine injection, examining the roles of the inflammatory markers myeloperoxidase (MPO), tumour necrosis factor alpha (TNF-α ), and vascular endothelial growth factor (VEGF) in nicotine-induced vascular damage and the protective effects of two known antioxidant agents, N-acetylcysteine (NAC) and vitamin E. Female Wistar rats were divided into four groups, each composed of nine rats: negative control group, positive control group, NACtreated group (500 mg/kg), and vitamin E-treated group (500 mg/kg). Nicotine was intraperitoneally injected at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Lung tissue samples were stained with hematoxylin-eosin (H&E) for histopathological assessments. Apoptosis level in endothelial cells was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Staining of cytoplasmic TNF-α and VEGF in endothelial cells, and perivascular MPO activity were evaluated by immunohistochemistry. The treatments with NAC and vitamin E significantly reduced the rate of nicotine-induced endothelial cell apoptosis. NAC and vitamin E significantly reduced the increases in the local production of TNF-α and VEGF, and perivascular MPO activity. This findings suggest that NAC can be as effective as vitamin E in protecting against nicotine-induced endothelial cell apoptosis. Human & Experimental Toxicology (2007) 26: 595—602.

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Experimental model to study the effect of nicotine in a random skin flap, in the rat

Cited by 8 publications

References 10 publications

Laser 830nm na viabilidade do retalho cutâneo de ratos submetidos à nicotina

Laser 830nm na viabilidade do retalho cutâneo de ratos submetidos à nicotina

The effects of erdosteine, N‐acetylcysteine and vitamin E on nicotine‐induced apoptosis of cardiac cells

Regulation of nicotine-induced apoptosis of pulmonary artery endothelial cells by treatment of N-acetylcysteine and vitamin E

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