Nicotine dose–concentration relationship and pregnancy outcomes in rat: Biologic plausibility and implications for future research

Hussein, Jabeen; Farkas, Svetlana; MacKinnon, Yolanda; Ariano, Robert E.; Sitar, Daniel S.; Hasan, Shabih U.

doi:10.1016/j.taap.2006.10.019

Cited by 35 publications

(30 citation statements)

References 46 publications

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“…A limitation of these studies was the route of nicotine dosing (via oral gavages, implantable osmotic minipump, subcutaneous intravenous injections, or parenteral bolus); these routes require high nicotine doses to achieve relevant plasma concentrations for heavy smokers that also cause maternal cardiovascular effects in rodents. Nicotine does not reproduce all the effects seen with cigarette smoke, leading us and others to believe that nicotine alone cannot cause the acute endothelial toxicity related to passive smoking (6) and that other constituents of cigarette smoke during pregnancy likely play a role in fetal growth restriction (29). It is important to note that the vascular effects reported here were observed 18 -19 h after the last smoke exposure.…”

Section: Discussionmentioning

confidence: 68%

“…Nicotine alone has previously been shown to reduce uterine blood flow in pregnant sheep and rats (8,11,42,43), mediated through release of epinephrine. However, some reports have shown no significant fetal growth restriction with nicotine or high levels of epinephrine (8,29,64). A limitation of these studies was the route of nicotine dosing (via oral gavages, implantable osmotic minipump, subcutaneous intravenous injections, or parenteral bolus); these routes require high nicotine doses to achieve relevant plasma concentrations for heavy smokers that also cause maternal cardiovascular effects in rodents.…”

Section: Discussionmentioning

confidence: 99%

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Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model

Gandley

Jeyabalan

Desai

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Smoking is associated with multiple adverse pregnancy outcomes, including fetal growth restriction. The objective of this study was to determine whether cigarette smoke exposure during pregnancy in a mouse model affects the functional properties of maternal uterine, mesenteric, and renal arteries as a possible mechanism for growth restriction. C57Bl/CJ mice were exposed to whole body sidestream smoke for 4 h/day. Smoke particle exposure was increased from day 4 of gestation until late pregnancy (day 16-19), with mean total suspended particle levels of 63 mg/m(3), representative of moderate-to-heavy smoking in humans. Uterine, mesenteric, and renal arteries from late-pregnant and virgin mice were isolated and studied in a pressure-arteriograph system (n = 23). Plasma cotinine was measured by ELISA. Fetal weights were significantly reduced in smoke-exposed compared with control fetuses (0.88 +/- 0.1 vs. 1.0 +/- 0.08 g, P < 0.02), while litter sizes were not different. Endothelium-mediated relaxation responses to methacholine were significantly impaired in both the uterine and mesenteric vasculature of pregnant mice exposed to cigarette smoke during gestation. This difference was not apparent in isolated renal arteries from pregnant mice exposed to cigarette smoke; however, relaxation was significantly reduced in renal arteries from smoke-exposed virgin mice. In conclusion, we found that passive cigarette smoke exposure is associated with impaired vascular relaxation of uterine and mesenteric arteries in pregnant mice. Functional maternal vascular perturbations during pregnancy, specifically impaired peripheral and uterine vasodilation, may contribute to a mechanism by which smoking results in fetal growth restriction.

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model

Gandley

Jeyabalan

Desai

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

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“…Altered apoptosis is suggested as a mechanism for other birth defects (Edwards, 1998), but has not yet been suggested as a mechanism for gastroschisis. Of interest, pup weight, placental weight, and organ weight are unaffected by nicotine dosing, suggesting that other by-products of cigarette smoking are responsible for the impact on fetal growth (Hussein et al, 2007). Though nicotine produces vasoconstriction, which may decrease overall blood flow and nutrient supply, other tobacco toxins may influence abnormal development of the ventral body wall, and therefore other pathogenic mechanisms should be considered.…”

Section: Discussionmentioning

confidence: 99%

A case control population‐based study investigating smoking as a risk factor for gastroschisis in Utah, 1997–2005

Feldkamp

Alder

Carey

2008

Birth Defects Research

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Though first trimester cigarette smoking was reported on birth certificates by more mothers of gastroschisis cases than controls, adjustment for confounders (maternal age and preconception BMI) and smoking misclassification suggests the association is weak. Despite a decrease in smoking prevalence among all women of childbearing years in Utah between 1997 and 2005, the prevalence of gastroschisis has not followed a similar trend.

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“…Indeed, some scientists believe that the potential neuroteratogenicity of nicotine is such that NRT should never be used at all in pregnancy and that even the heaviest of maternal smokers would expose their fetuses to increased risk by using NRT instead of smoking while pregnant. (Ginzel et al, 2007) However, this is not a consensus view and others dispute that appropriate doses of nicotine were used in the original rodent studies, believing that these were far higher than should have been used to draw conclusions about nicotinerelated harm from either using NRT or smoking by humans (Hussein et al, 2007).…”

Section: Safetymentioning

confidence: 99%

Reducing harm from tobacco smoke exposure during pregnancy

Coleman

2008

Birth Defects Research Pt C

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In addition to the health risks that maternal tobacco smoke exposure in pregnancy poses to women, this is a cause of substantial fetal morbidity and mortality. In pregnancy, maternal tobacco smoke exposure can arise because women either smoke or are passively exposed to environmental tobacco smoke as a consequence of other's smoking. This article discusses the scope for clinicians to help reduce both types of tobacco smoke exposure in pregnancy, with a specific focus on available and effective interventions for smoking cessation by pregnant women. Behavioral support with smoking cessation is the only intervention that has been proven to encourage smoking cessation in pregnancy and reduces smoking rates in late pregnancy by 6 to 7%. There are physiological reasons to suspect that nicotine replacement therapy (NRT) will be less or (in)effective for smoking cessation in pregnancy when compared with its use by nonpregnant smokers. However, there are also strong theoretical reasons to suspect that NRT is likely to be safer than continued smoking in pregnancy. Consequently, this article reviews evidence for the safety and effectiveness of NRT when used for smoking cessation in pregnancy and recommendations concerning the use of NRT in pregnancy are presented.

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Nicotine dose–concentration relationship and pregnancy outcomes in rat: Biologic plausibility and implications for future research

Cited by 35 publications

References 46 publications

Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model

Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model

A case control population‐based study investigating smoking as a risk factor for gastroschisis in Utah, 1997–2005

Reducing harm from tobacco smoke exposure during pregnancy

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