Diminished Prostacyclin Formation in Umbilical Arteries of Babies Born to Women Who Smoke

Dadak, Ch.; Leithner, C; Sinzinger, H.; Silberbauer, K

doi:10.1016/s0140-6736(81)90024-6

Cited by 74 publications

(14 citation statements)

References 5 publications

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“…The biological variations in the capacity for prostacyclin formation in the same tissue from different subjects are considerable. The results of the bioassay technique used here for analysis of PGU-like activity varies within relatively wide ranges, but are of the same magnitude as those in other similar studies [13][14][15]. Using thin-layer chromatog raphy, Dadak et al, [16] have shown a re duced conversion of arachidonic acid to prostacyclin in both umbilical arteries and veins of infants to smoking mothers com pared with a non-smoking control group.…”

Section: Discussionsupporting

confidence: 68%

Prostacyclin-Like Activity in Umbilical Arteries Is Dose-Dependently Reduced by Maternal Smoking and Related to Nicotine Levels

Ahlsten¹,

Ewald²,

Tuvemo³

1990

Neonatology

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The influence of maternal smoking on the formation of prostacyclin-like activity in human umbilical arteries was studied in 84 unselected term deliveries. In arteries from infants of nonsmoking mothers the prostacyclin-like activity measured by a bioassay technique amounted to 81 ± 37 ng/g (mean ± SD), and in those from smokers to 67 ± 35 ng/g (p < 0.05). When smokers were divided into those smoking 10 cigarettes daily or more and those smoking 1–9 cigarettes per day, only arteries of infants of the heavier smokers showed a significantly reduced prostacyclin-like activity (56 ± 27 ng/g; p < 0.02). Nicotine and cotinine levels were weakly inversely correlated to prostacyclin-like activity (p < 0.05). Reduced prostacyclin production in umbilical arteries implies reduced capacity for vasodilation and lowered defence against fetal hypoxia in heavy smokers.

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Section: Discussionsupporting

confidence: 68%

Prostacyclin-Like Activity in Umbilical Arteries Is Dose-Dependently Reduced by Maternal Smoking and Related to Nicotine Levels

Ahlsten¹,

Ewald²,

Tuvemo³

1990

Neonatology

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“…If we assume that the vascular tone of cerebral arteries is increased after prenatal smoke exposure, this could be explained by alterations of the synthesis of endothelial derived vaso-active factors that play an important role in the regulation of the cerebral circulation [9]. This speculation would be in agreement with the observation of a reduced synthesis of prostacyclin in umbilical arteries from newborns of smoking mothers [1,6].…”

Section: Discussionmentioning

confidence: 58%

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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“…1) [124], Mechanical or chemical pertubation of cell mem branes results in the formation of PGI2 [125], Pulsatile pressure, bradykinins, serotonin, PDGF, IL-1, and adenine nucleotides stimulate its production [126]. The capacity of endothelial cells to generate PGI2 decreases with age, smok ing [127], diabetes, and atherosclerosis. In addition, infu sions of PGI2 have been shown to prevent intimal thicken ing [125] and directly inhibit the proliferation of cultured vascular smooth muscle cells [128].…”

Section: Proendothelial Agentsmentioning

confidence: 99%