Blood levels of nicotine and physiological effects after inhalation of tobacco smoke

Isaac, P.F.; Rand, M. J.

doi:10.1016/0014-2999(69)90035-1

Cited by 49 publications

(23 citation statements)

References 12 publications

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“…Blood levels of nicotine and cotinine (a breakdown product of nicotine) were measured every two weeks and demonstrated the controlled systemic release of nicotine (Table I). The nicotine levels in our study were consistent with levels that have been shown to delay fracture healing and were comparable with those in an adult who smokes twenty to thirty cigarettes a day [20][21][22] . The rats were killed at ten, twenty-eight, and fifty-six days, with twelve rats being killed at each time-point in each group.…”

Section: Animal Injury Modelsupporting

confidence: 87%

Nicotine Delays Tendon-to-Bone Healing in a Rat Shoulder Model

Galatz¹,

SILVA²,

Rothermich³

et al. 2006

The Journal of Bone and Joint Surgery-American Volume

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Section: Animal Injury Modelsupporting

confidence: 87%

Nicotine Delays Tendon-to-Bone Healing in a Rat Shoulder Model

Galatz¹,

SILVA²,

Rothermich³

et al. 2006

The Journal of Bone and Joint Surgery-American Volume

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“…Nicotine also acts directly on the small vessels producing vasoconstriction, systemic venoconstriction and increasing coronary vascular resistance 7,15 . Therefore, blood supply is primarily affected by nicotine.…”

Section: Discussionmentioning

confidence: 99%

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

Saldanha¹,

Pimentel²,

Casati³

et al. 2004

Braz. oral res.

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ABSTRACT:The objective of this study was to investigate the histometric impact of nicotine on bone regeneration of surgically created alveolar ridge defects in dogs. Sixteen mongrel dogs were used. One defect was surgically created unilaterally in the mandible, and left to heal spontaneously. The animals were randomly assigned to one of the following groups: Group 1 -control (n = 8) and Group 2 -subcutaneous nicotine administration (2 mg/kg) twice a day (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. Bone height (BH), bone width (BW), bone density (BD), and bone area (BA) of the newly-formed bone were evaluated. Intergroup analysis (Mann-Whitney rank sum test) showed that regardless of the presence of nicotine, no significant differences were observed regarding bone width (BW), bone area (BA) and bone height (BH) (p > 0.05). On the other hand, it was demonstrated that nicotine administration significantly influenced the proportion of mineralized tissue within the limits of the newly-formed bone (BD) (p < 0.001). Within the limits of the present study, it can be concluded that nicotine might affect but not prevent bone healing in defects left to heal spontaneously. DESCRIPTORS: Smoking; Nicotine; Tobacco; Bone regeneration. RESUMO:O objetivo do presente estudo foi avaliar histometricamente a influência da nicotina sobre a regeneração óssea de defeitos criados cirurgicamente em rebordos alveolares edêntulos de cães. Defeitos ósseos foram criados cirurgicamente em um dos lados da mandíbula de dezesseis cães e foram deixados para que curassem espontaneamente. Os animais foram aleatoriamente designados para um dos seguintes grupos: Grupo 1 -controle (n = 8) e Grupo 2 -administração subcutânea de nicotina (2 mg/kg) duas vezes ao dia durante 4 meses (n = 8). Os animais foram sacrificados, e secções semi-seriadas descalcificadas, obtidas. Os parâmetros histométricos avaliados foram altura, largura, área e densidade do tecido ósseo neoformado. A análise intergrupos (Mann-Whitney "rank sum test") demonstrou que a administração de nicotina não influenciou altura, largura e área de tecido ósseo neoformado (p > 0,05). Entretanto, a administração de nicotina influenciou significativamente a densidade do tecido ósseo neoformado (p < 0,001). Dentro dos limites do presente estudo, pode-se concluir que a nicotina pode afetar, mas não impedir a regeneração de defeitos ósseos criados cirurgicamente em mandíbulas edêntulas de cães.

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“…Unfortunately, most of these reports use abnormally high NIC concentrations that are not normally found in humans, and they administer NIC in a bolus injection. To accurately reproduce the most common use of NIC-containing products (i.e., smoking), one must administer NIC slowly over several minutes to achieve a concentration similar to that seen in the plasma of smokers (29). Our study achieves this by acutely administering NIC in a concentration (29,52) and time frame commonly seen in cigarette smokers.…”

mentioning

confidence: 89%

“…To accurately reproduce the most common use of NIC-containing products (i.e., smoking), one must administer NIC slowly over several minutes to achieve a concentration similar to that seen in the plasma of smokers (29). Our study achieves this by acutely administering NIC in a concentration (29,52) and time frame commonly seen in cigarette smokers. We also examined the effects of chronic, continuous NIC use (i.e., 4 mo) on hemodynamics and cardiac remodeling in NTG and Tm175 mice.…”

mentioning

confidence: 89%

“…This tubing was connected to a 250-l glass syringe mounted on a model 355 microinfusion pump (Sage Instruments, Cambridge, MA), which allowed for precise delivery of NIC hydrogen tartrate salt in various doses: 2.5, 5, and 10 ng·g Ϫ1 ·min Ϫ1 delivered over 8 min at 1 l/min. The NIC concentrations used (20,40, and 80 ng/g) correlate to the amount of NIC absorbed by a human after smoking 0.25, 0.5, or 1 cigarette (20,29,47,52,55). In control experiments, we utilized saline for femoral injections.…”

Section: In Situ Measurements For Acute and Chronic Nic Studiesmentioning

confidence: 99%

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Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

Gaffin

Chowdhury

Alves

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Gaffin RD, Chowdhury SA, Alves MS, Dias FA, Ribeiro CT, Fogaca RT, Wieczorek DF, Wolska BM. Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, ␣-tropomyosin D175N. Am J Physiol Heart Circ Physiol 301: H1646-H1655, 2011. First published July 8, 2011 doi:10.1152/ajpheart.00277.2010.-The effects of nicotine (NIC) on normal hearts are fairly well established, yet its effects on hearts displaying familial hypertrophic cardiomyopathy have not been tested. We studied both the acute and chronic effects of NIC on a transgenic (TG) mouse model of FHC caused by a mutation in ␣-tropomyosin (Tm; i.e., ␣-Tm D175N TG, or Tm175). For acute effects, intravenously injected NIC increased heart rate, left ventricular (LV) pressure, and the maximal rate of LV pressure increase (ϩdP/dt) in non-TG (NTG) and Tm175 mice; however, Tm175 showed a significantly smaller increase in the maximal rate of LV pressure decrease (ϪdP/dt) compared with NTGs. Western blots revealed phosphorylation of phospholamban Ser16 and Thr17 residue increased in NTG mice following NIC injection but not in Tm175 mice. In contrast, phosphorylation of troponin I at serine residues 23 and 24 increased equally in both NTG and Tm175. Thus the attenuated increase in relaxation in Tm175 mice following acute NIC appears to result primarily from attenuated phospholamban phosphorylation. Chronic NIC administration (equivalent to smoking 2 packs of cigarettes/day for 4 mo) also increased ϩdP/dt in NTG and Tm175 mice compared with chronic saline. However, chronic NIC had little effect on heart rate, LV pressure, ϪdP/dt, LV wall and chamber dimensions, or collagen content for either group of mice. in vivo pressure recordings; phospholamban; phosphorylation; cardiac remodeling NUMEROUS STUDIES HAVE TESTED the adverse effects of smoking on cardiovascular health in both healthy and diseased hearts (reviewed in Ref. 5). However, many of these adverse effects may be attributable to the "tar" and/or carbon monoxide in cigarette smoke. Nicotine (NIC) is widely heralded as the addictive component of cigarettes, cigars, and pipe tobacco (6, 7), and its impact alone on cardiovascular disease is gaining more recognition due to the presence of a myriad of smokeless tobacco products (reviewed in Ref. 46). Yet, to the best of our knowledge, its impact on familial hypertrophic cardiomyopathies (FHCs) has not been studied.FHCs are defined as autosomal dominant disorders that result in numerous cardiac maladies including hypertrophy, diastolic dysfunction, fibrosis, myocyte disarray, and arrhythmias (9, 34). They are considered to be a leading cause of sudden cardiac death in young athletes (10,32,35) and have a prevalence of 1:500 when familial and nonfamilial forms are considered together (16). FHCs have been described as a "disease of the sarcomere" since the majority of cases have been linked to mutations in sarcomeric proteins such as myosin heavy chain, troponin T, myosin-binding protein C, and ␣-tropomyosin (Tm; Refs. 9, 21, 54, 64). We have ...

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Blood levels of nicotine and physiological effects after inhalation of tobacco smoke

Cited by 49 publications

References 12 publications

Nicotine Delays Tendon-to-Bone Healing in a Rat Shoulder Model

Nicotine Delays Tendon-to-Bone Healing in a Rat Shoulder Model

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

Effects of nicotine administration in a mouse model of familial hypertrophic cardiomyopathy, α-tropomyosin D175N

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