Effects of maternal smoking on circulating catecholamine levels and fetal heart rates

Quigley, M. E.; Sheehan, Kate L.; Wilkes, Mahlon M.; Yen, S. S. C.

doi:10.1016/0002-9378(79)90019-x

Cited by 111 publications

(51 citation statements)

References 29 publications

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“…We do not believe that the differences in CBFVs observed in our study between infants of smoking mothers and controls can be explained by such acute effects of nicotine, catecholamines [17], or carbon monoxide [11], for both nicotine and carbon monoxide have a half-life too short to explain a prolonged influence in infants 20 h or more after birth. Also, if nicotine were directly responsible for the increased CBFVs, concomitant catecholamine-mediated changes in BP and heart rate should be expected but could not be observed in this study.…”

Section: Discussionmentioning

confidence: 57%

Increased cerebral blood flow velocities in newborn infants of smoking mothers

et al. 1993

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Abstract. Cerebral blood flow velocities (CBFV) weremeasured by the pulsed Doppler method in 41 infants of smoking mothers and in 59 apparently healthy control infants. Although gestational age, birth weight, and systolic blood pressure were lower in infants exposed to tobacco smoke prenatally, systolic (65 + 11 vs. 47 + 12cm/s, mean_+SD; P<0.001), mean (36+6 vs. 25+6cm/s; P< 0.001), and diastolic (17 + 4 vs 13 + 4cm/s; P < 0.001) CBFVs in the anterior cerebral artery were significantly higher when compared to control infants. Similar differences were seen in the internal carotid and in the basilar arteries. Multiple regression analysis did not reveal differences .other than maternal smoking to explain these observations. We conclude that prenatal tobacco smoke exposure is related to increased CBFVs in newborn infants. Further studies should determine whether this relation is not only statistical but causal and whether increased CBFVs are an indicator of prolonged effects of prenatal tobacco smoke exposure.

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Section: Discussionmentioning

confidence: 57%

Increased cerebral blood flow velocities in newborn infants of smoking mothers

et al. 1993

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“…No feto, a nicotina reduz a perfusão placentária devido a sua ação vasoconstritora, além de atravessar facilmente as barreiras placentária e hematoencefálica, atingindo rapidamente o feto, podendo causar danos diretos sobre o mesmo 33 . Quingley et al 34 responsabilizaram a nicotina pelo aumento da freqüência cardíaca fetal que ocorre após o uso do cigarro pela gestante. A ação da nicotina seria através do aumento da produção de catecolaminas, responsáveis por vasoconstrição e diminuição da perfusão uterina.…”

Section: Ação Na Gestação Mecanismos Referênciaunclassified

Influência do tabagismo na fertilidade, gestação e lactação

Mello¹,

Pinto²,

Botelho³

2001

J. Pediatr. (Rio J.)

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Objective: to decribe the influence of smoking on different phases of the reproductive process, fecundation, pregnancy and lactation, drawing special attention to the mechanisms of action of the main toxic components found in cigarettes. To suggest prophylactic measures for environmental control and how to reduce children's exposure to tobacco smoke.Methods: nonsystematic literature review using MEDLINE database.Results: smoking has a negative effect on different phases of the reproduction process, by direct action of main toxic components, nicotine and carbon monoxide. Smoking reduces fertility, compromises the length of gestation and infant birthweight. Smoking mothers also have reduced breast milk production and shorter lactation, which affects infant weight gain through unclear mechanisms in which prolactin may probably be involved.Conclusions: smoking compromises reproductive function quality in different phases, acting mainly on intrauterine and extrauterine development of infants. Since during pregnancy and lactation women are in closer contact with health professionals, antismoking campaigns should be especially addressed to this period.J Pediatr (Rio J) 2001; 77 (4): 257-64: smoking, fertility, pregnancy, lactation, breast feeding. ResumoObjetivo: descrever a influência do tabagismo nas diferentes fases do processo reprodutivo, fecundação, gestação e lactação, destacando os mecanismos de ação dos principais componentes tóxicos do cigarro nestas fases. Sugerir medidas profiláticas de controle ambiental e de como reduzir a exposição da criança à fumaça do tabaco.Métodos: revisão bibliográfica não sistemática sobre os temas abordados, utilizando-se da base de dados do MEDLINE.Resultados: o tabagismo atua negativamente nas diferentes fases da reprodução, por ação direta de seus principais componentes tóxicos, a nicotina e o monóxido de carbono. Reduz a taxa de fertilidade, compromete a duração da gestação e o peso do concepto. Também diminui a produção de leite da nutriz fumante e o tempo de lactação, comprometendo o ganho de peso da prole, por mecanismos ainda não bem compreendidos, nos quais a prolactina pode estar envolvida.Conclusões: os efeitos do tabagismo comprometem a qualidade da função reprodutiva em diferentes fases, por atuar principalmente sobre o desenvolvimento do concepto, tanto na fase intra quanto na fase extra-uterino. Por ser um período de contato mais freqüente da mulher fumante com o profissional de saúde, a gestação e a lactação deveriam ser alvo especial de campanhas antitabágicas.J Pediatr (Rio J) 2001; 77 (4): 257-64: tabagismo, fertilidade, gestação, lactação, aleitamento materno. Influência do tabagismo na fertilidade, gestação e lactaçãoThe influence of smoking on fertility, pregnancy and lactation Paulo Roberto Bezerra de Mello 1 , Gilberto Rodrigues Pinto 2 , Clovis Botelho 3A fumaça do cigarro no ambiente é derivada de duas origens: fumaça central (FC) e fumaça periférica (FP). A fumaça central é formada quando o fumante traga o cigarro, é produzida com altas temperat...

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“…Nicotine is one of these adverse components [8] . It is known to cross the placenta and can be detected in fetal circulation, where it can affect the fetus in several ways [9][10][11][12] . Our previous studies [13] found that prenatal nicotine exposure (PNE) caused IUGR in rats; the fetuses were overexposed to maternal GC, and the development of the fetal HPA axis was inhibited.…”

Section: Introductionmentioning

confidence: 99%

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Xia

Shen

et al. 2013

Acta Pharmacol Sin

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Aim: Prenatal nicotine exposure (PNE) alters the hypothalamic-pituitary-adrenocortical (HPA) axis-associated neuroendocrine metabolic programming in intrauterine growth retardation offspring rats. In this study we aimed to clarify the susceptibility to metabolic diseases of PNE offspring rats fed a high-fat diet. Methods: Maternal Wistar rats were injected with nicotine (1.0 mg/kg, sc) twice per day from gestational day 11 until full-term delivery, and all pups were fed a high-fat diet after weaning and exposed to unpredictable chronic stress (UCS) during postnatal weeks 18-20. Blood samples were collected before and after chronic stress, and serum ACTH, corticosterone, glucose, insulin, total cholesterol, triglyceride and free fatty acids levels were measured. The hypothalamus, pituitary gland and liver were dissected for histological studies. Results: UCS significantly increased the serum ACTH, corticosterone and insulin levels as well as the insulin resistant index without changing the serum glucose, total cholesterol, triglyceride and free fatty acids levels in adult offspring rats without PNE. The body weight of PNE offspring rats presented a typical "catch-up" growth pattern. PNE not only aggravated the UCS-induced changes in the HPA axis programmed alteration (caused further increases in the serum ACTH and corticosterone levels), but also significantly changed the glucose and lipid metabolism after UCS (caused further increases in the serum glucose level and insulin resistant index, and decrease in the serum free fatty acids). The effects of PNE on the above indexes after UCS showed gender differences. Pathological studies revealed that PNE led to plenty of lipid droplets in multiple organs. Conclusion: PNE enhances not only the HPA axis, but also the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet after UCS in a gender-specific manner and enhances the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet.

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Effects of maternal smoking on circulating catecholamine levels and fetal heart rates

Cited by 111 publications

References 29 publications

Increased cerebral blood flow velocities in newborn infants of smoking mothers

Increased cerebral blood flow velocities in newborn infants of smoking mothers

Influência do tabagismo na fertilidade, gestação e lactação

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

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