Carbon monoxide poisoning in pregnancy

Aubard, Y.; Magne, Isabelle

doi:10.1111/j.1471-0528.2000.tb11078.x

Cited by 76 publications

(57 citation statements)

References 27 publications

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“…3,4 This CO concentration is reported to result in carboxy-hemoglobin level similar to those attained in a moderate-heavy tobacco smoker. 1 The duration of gestation was calculated starting from the day on which sperm was present in vaginal smears, taken on the morning at 09:00 hours after placement of two female with a single male rat. The day was designated as day 0 of gestation and for all rats the duration was 20-21 days.…”

Section: Materials and Methods Co Treatment Of The Animalsmentioning

confidence: 99%

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Prenatal exposure to carbon monoxide delays postnatal cardiac maturation

Sartiani

Stillitano

Luceri

et al. 2010

Laboratory Investigation

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Prenatal exposure to toxicants, such as maternal smoking, may impair cardiovascular autonomic maturation in infants. We recently showed that exposure of pregnant rats to a mild concentration of carbon monoxide (CO), a component of cigarette smoke, delays postnatal electrophysiological maturation of ventricular myocytes from newborns rats, likely predisposing to life-threatening arrhythmias. To get a comprehensive view of developmental molecular abnormalities induced, at cardiac level, by prenatal CO exposure, we used microarray analysis approach on the rat heart at 4, 7 and 20 days postnatal life. The relationship between molecular and functional alterations was investigated by assessing the ventricular expression of f-current, an electrophysiological marker of immature cardiac phenotype. Rats were prenatally exposed to 0 (CTR) or 150 p.p.m. CO and mRNA obtained from ventricular samples. Differential analysis and biological pathway analysis of microarray data were performed by using Newton's approach and the GENMAPP/MAPPFinder, respectively. The real-time RT-PCR reactions were performed by TaqMan probe-based chemistry. Freshly isolated patch-clamped ventricular cardiomyocytes were used to measure I f . Genes and pathways controlling cell cycle and excitation-contraction coupling were significantly modified in CO-exposed rats. The higher effect was observed in cardiomyocytes harvested from 7-day-old rats, in which mRNA expression for crucial sarcomeric proteins (myosin and actin subunits, troponin I), transporters (Ca 2 þ transporting ATPase) and enzymes (aldolase) were significantly downregulated. Accordingly, the molecular and functional expression of f-channels, which represents a marker of fetal ventricular phenotype, was transiently greater in CO-exposed rats ( þ 200%) than in control ones. In conclusion, our study provides new insights into the molecular and functional mechanisms underlying cardiac maturation and its impairment by prenatal exposure to toxic components of smoking, such as CO.

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Section: Materials and Methods Co Treatment Of The Animalsmentioning

confidence: 99%

“…Fetal hemoglobin has a fourfold higher affinity for CO compared with the adult form, 1 thus increasing fetal exposure to CO damage. Exposure of pregnant rats to 150 p.p.m.…”

mentioning

confidence: 99%

Prenatal exposure to carbon monoxide delays postnatal cardiac maturation

Sartiani

Stillitano

Luceri

et al. 2010

Laboratory Investigation

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“…1 Tobacco smoking is an important source of chronic exposure to carbon monoxide (CO): CO contained in cigarette smoke (Ϸ4%) easily crosses the placental barrier by passive diffusion, causing a 4-fold increase in carboxyhemoglobin levels in the umbilical cord blood. 2 The consequent chronic fetal hypoxia may retard fetal growth 2 and alter the physiological development of organs and tissues, especially those most susceptible to hypoxia damage, including the brain. 3,4 Alterations in the autonomic nervous system in infants born from smoking mothers have been reported.…”

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confidence: 99%

Prenatal Exposure to Carbon Monoxide Affects Postnatal Cellular Electrophysiological Maturation of the Rat Heart

et al. 2004

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Background-Maternal smoking is an independent risk factor for sudden infant death syndrome (SIDS). Carbon monoxide (CO) is a major component of smoke. No information is available about the effect of CO and/or smoking on postnatal maturation of the heart. The aim of this study was to investigate the effect of prenatal exposure to CO on cellular electrophysiological maturation in male Wistar rats. Methods and Results-The patch-clamp technique was used to measure action potential (AP) and ionic currents (I to and I Ca,L ) from rat ventricular myocytes. During growth, AP duration measured at Ϫ20 and Ϫ50 mV (APD Ϫ20 and APD Ϫ50 ) decreased progressively in both groups; the process was significantly delayed in rats exposed prenatally to 150 ppm CO: At 4 weeks, APD Ϫ20 and APD Ϫ50 were 89.5Ϯ18.2 and 147.7Ϯ24.5 ms in CO (nϭ13)

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“…This is due to several factors, includes a central respiratory stimulation, increased sensitivity of peripheral chemoreceptors, and increased oxygen consumption during pregnancy. It has been hypothesized, therefore, that pregnant women are at increased risk of CO poisoning [41]. However, in an elegant and thorough study of volunteers exposed to ambient CO of different concentrations for various lengths of time while sedentary and while exercising, Peterson and Stewart for no difference in COHb concentrations with exercise [42].…”

Section: Carbon Monoxide Exposure In Pregnancymentioning

confidence: 99%

Neurologic and Pregnancy Effects of Carbon Monoxide Exposure

Bird¹

2017

Toxicol Open Access

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Carbon monoxide exposure remains a public health concern worldwide. Despite the burden that carbon monoxide exerts, significant controversy exists regarding optimal treatment of exposed persons. Particular controversy exists around neurologic effects of carbon monoxide exposure, how best to evaluate for neurocognitive dysfunction, and effects on the fetus of pregnant women. This review focuses on the mechanism of injury from carbon monoxide, and summarizes the data regarding neurocognitive dysfunction and fetal effects of exposure.

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Carbon monoxide poisoning in pregnancy

Cited by 76 publications

References 27 publications

Prenatal exposure to carbon monoxide delays postnatal cardiac maturation

Prenatal exposure to carbon monoxide delays postnatal cardiac maturation

Prenatal Exposure to Carbon Monoxide Affects Postnatal Cellular Electrophysiological Maturation of the Rat Heart

Neurologic and Pregnancy Effects of Carbon Monoxide Exposure

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