Effects of prenatal carbon monoxide exposure on cardiac development

Fechter, Laurence D.; Thakur, M.L.; Miller, Brady L.; Annau, Zoltan; Srivastava, Uma

doi:10.1016/0041-008x(80)90070-8

Cited by 14 publications

(2 citation statements)

References 21 publications

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“…A first experiment was to determine if perinatal alcohol exposure might affect homing behavior, which is a simple form of learning based on ultrasonic and olfactory cues (Altman and Sudarshan 1975;Fechter and Annau 1980). In this regard, it could be hypothesized that the decreased rate of ultrasonic emission observed in sP-A pups exposed to alcohol during development (Tattoli et al 2001) might influence their performance in this test.…”

mentioning

confidence: 99%

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Cagiano

Cassano

Coluccia

et al. 2002

Neuropsychopharmacology

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and neurochemical effects of perinatal alcohol exposure (3% v/v solution from Day 15 of gestation to Day 7 after parturition) have been investigated in Sardinian alcohol-preferring (sP) and alcohol-nonpreferring (sNP) Previous data suggest that genetic factors could contribute to differences in susceptibility to alcohol-related neurodevelopmental disorders (ARNDs) (Gilliam et al. 1987;Gilliam and Irtenkauf 1990;Govoni et al. 1994;Hannigan 1996;Riley and Lochry 1982;Riley et al. 1993). A recent study in the present series has shown that offspring of Sardinian alcohol-preferring (sP) and Sardinian alcohol-nonpreferring (sNP) rats, selectively bred (from Wistar rats) for opposite alcohol preference and consumption, exhibited a different behavioral profile in response to perinatal exposure to this drug of

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mentioning

confidence: 99%

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Cagiano

Cassano

Coluccia

et al. 2002

Neuropsychopharmacology

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“…Previous findings have shown that prenatal exposure to CO, at concentrations (75–150 p.p.m.) below those associated with gross malformations and/or overt neurotoxic effects, induces a variety of neurobehavioural abnormalities in rat offspring including lower behavioural activity levels through preweaning, delayed development of homing behaviour and negative geotaxis, altered ontogeny of emotional responsiveness and permanent cognitive deficits (Fechter & Annau, 1977, 1980; Mactutus & Fechter, 1984, 1985; Di Giovanni et al , 1993; De Salvia et al , 1995).…”

Section: Introductionmentioning

confidence: 99%

Effects of prenatal exposure to low concentrations of carbon monoxide on sexual behaviour and mesolimbic dopaminergic function in rat offspring

Cagiano

Ancona

Cassano

et al. 1998

British J Pharmacology

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1 Inhalation of low concentrations of carbon monoxide (CO) by pregnant rats (75 and 150 p.p.m. from day 0 to day 20 of gestation) leads to changes in mesolimbic dopaminergic transmission associated with an impairment of sexual behaviour in male o spring. 2 Eighty day old males exposed in utero to CO (150 p.p.m.) exhibited a signi®cant increase in mount/ intromission latency as well as a signi®cant decrease in mount/intromission frequency. A signi®cant decrease in ejaculation frequency was also found in CO (150 p.p.m.)-exposed animals. 3 The acute administration of amphetamine, at a dose (0.5 mg kg 71 s.c.) stimulating copulatory activity in control rats, failed to reduce mount/intromission latency and did not increase mount frequency in 80-day o spring exposed to CO (150 p.p.m.) during gestation. 4 These behavioural alterations were paralleled by neurochemical changes (in vivo microdialysis) showing that prenatal CO exposure, at concentrations (150 p.p.m.) that did not a ect basal extracellular levels of dopamine in the nucleus accumbens, blunted the amphetamine (0.5 mg kg 71 s.c.)-induced increase in dopamine release in 80-day old male rats. 5 No signi®cant changes in either behavioural or neurochemical parameters were observed in 10-month old rats exposed prenatally to CO. 6 Since the alterations in sexual behaviour and dopaminergic transmission have been produced by prenatal exposure to CO levels resulting in maternal blood carboxyhaemoglobin concentrations equivalent to those maintained by human cigarette smokers, the present data further point out the large risk that the smoking mother poses for her o spring.

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Trauma in pregnancy

Vaizey

Jacobson²,

Cross

1994

Journal of British Surgery

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Trauma is a major cause of maternal death in pregnancy. The pregnant woman who has been involved in an episode leading to her arrival in an accident and emergency department presents with specific problems that often require specialist attention. The correct initial management of such patients should not be beyond the capabilities of an average trauma team and such management is clearly taught as part of the Advanced Trauma Life Support course now available in the UK. This review outlines the physiological changes associated with pregnancy that become important during resuscitation and definitive care. It discusses the presentation and management of specific problems, and the safety--or otherwise--of commonly administered drugs. Only the initial resuscitation of the patient is considered; specialist obstetric care is beyond the scope of the article.

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Effects of prenatal carbon monoxide exposure on cardiac development

Cited by 14 publications

References 21 publications

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Effects of prenatal exposure to low concentrations of carbon monoxide on sexual behaviour and mesolimbic dopaminergic function in rat offspring

Trauma in pregnancy

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