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asphyxia/nicotine

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Prenatal nicotine exposure increases hyperventilation in α4-knock-out mice during mild asphyxia.

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Prenatal nicotine exposure alters breathing and ventilatory responses to stress through stimulation of nicotine acetylcholine receptors (nAChRs). We tested the hypothesis that α4-containing nAChRs are involved in mediating the effects of prenatal nicotine exposure on ventilatory and metabolic
Perinatal asphyxia (15-22 min) was induced to male Sprague-Dawley rat pups during the last day of gestation and the surviving pups were sacrificed at 4 weeks of age. Brain sections were stained for tyrosine hydroxylase immunoreactivity and Cresyl violet. With increasing duration of perinatal
In the present study, the effects of nicotine treatment on the changes induced by perinatal asphyxia in exploratory and D-amphetamine-induced behaviour, and in the number of brain tyrosine hydroxylase-immunoreactive nerve cell bodies were investigated in four-week-old male rats. Asphyxia was induced

[Historical vignette (2). Asphyxia caused by chewing tobacco during chloroform anesthesia].

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An Analytical Inquiry into the Causes of the Proscription of Tobacco in Cases of Asphyxia.

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Nicotine in a small-to-moderate dose does not cause a significant increase in plasma catecholamine levels in newborn piglets.

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BACKGROUND Nicotine has a wide range of effects. Several studies are being undertaken investigating the positive effects on inflammation and apoptosis. Recently, nicotine has been investigated in a piglet model of perinatal asphyxia, where the question has been raised whether nicotine's effect on

Effects of nicotine infusion on striatal glutamate and cortical non-protein-bound iron in hypoxic newborn piglets.

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BACKGROUND Perinatal asphyxia triggers a large cascade of mechanisms leading to brain damage. Release of glutamate and increased oxidative stress play substantial roles. Non-protein-bound iron (NPBI), which contributes to the production of free radical species through the Fenton reaction, increases
Brain-derived neurotrophic factor (BDNF) is highly expressed in the developing brain. It has anti-apoptotic abilities, and protects the neonatal brain. In experimental settings in adult animals, pre-treatment with nicotine has shown increased BDNF levels, indicating a possible contribution to

Prenatal Exposure to Environmental Tobacco Smoke and Hyperactivity Behavior in Chinese Young Children.

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This study aimed to examine the association between prenatal environmental tobacco smoke (ETS) exposure and hyperactivity behaviors in young children. A cross-sectional study was undertaken among 21,243 participants from all of the kindergartens in Longhua District of Shenzhen, China. Multivariate
OBJECTIVE The aim of this study was to evaluate the effects of maternal nicotine exposure during gestation on injury severity of small intestine in the newborn rats subjected to hypoxia-reoxygenation and cold stress. METHODS A total of 21 Sprague-Dawley pregnant rats were divided into 3 equal
A 31-year-old female was found dead with 18 nicotine transdermal system patches taped to her upper body and a plastic bag taped over her nose and mouth (the cause of death was ruled asphyxiation). Nicotine concentrations in biological fluids and tissues were analyzed using a liquid-liquid extraction

Pre- and early postnatal nicotine exposure exacerbates autoresuscitation failure in serotonin-deficient rat neonates.

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CONCLUSIONS Sudden infant death syndrome (SIDS) is one of the leading causes of death during the first year of life and abnormalities linked to serotonin (5-HT) have been identified in many SIDS cases. Cigarette smoking and associated exogenous stressors, e.g. developmental nicotine exposure, may

Threshold levels of maternal nicotine impairing protective responses of newborn rats to intermittent hypoxia.

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Experiments were carried out to determine the threshold level of maternal nicotine that impairs protective responses of rat pups to hypoxia. From days 6 or 7 of gestation, pregnant rats received either vehicle or nicotine (1.50, 3.00, or 6.00 mg of nicotine tartrate. kg body wt(-1).day(-1)) or
BACKGROUND Perinatal asphyxia is a major concern in perinatal medicine. Resuscitation and ways to prevent and minimize adverse outcomes after perinatal asphyxia are subject to extensive research. OBJECTIVE In this study we hypothesized that, prior to hypoxia, intravenously administered nicotine

Cardiorespiratory effects of nicotine exposure during development.

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Exposure to tobacco smoke is a major risk factor for the sudden infant death syndrome. Nicotine is thought to be the ingredient in tobacco smoke that is responsible for a multitude of cardiorespiratory effects during development, and pre- rather than postnatal exposure is considered to be most
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