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Oldal 1 tól től 512 eredmények
Brain-derived neurotrophic factor (BDNF) and TrkB in the piglet brainstem after post-natal nicotine and intermittent hypercapnic hypoxia.
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Brain-derived neurotrophic factor (BDNF) and its receptor TrkB play a significant role in the regulation of cell growth, survival and death during central nervous system development. The expression of BDNF and TrkB is affected by noxious insults. Two insults during the early post-natal period that
Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome.
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Maternal cigarette smoking has a high correlation with sudden Infant Death Syndrome, a condition in which cardiorespiratory failure occurs during an hypoxic episode, as in sleep apnea. Pregnant rats were given nicotine infusions of 2 or 6 mg/kg/day throughout gestation, regimens that produce plasma
Characterization of slowly inactivating KV{alpha} current in rabbit pulmonary neuroepithelial bodies: effects of hypoxia and nicotine.
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Pulmonary neuroepithelial bodies (NEB) form innervated cell clusters that express voltage-activated currents and function as airway O(2) sensors. We investigated A-type K(+) currents in NEB cells using neonatal rabbit lung slice preparation. The whole cell K(+) current was slowly inactivating with
Nicotine reduces mortality of developing rats exposed to high-altitude hypoxia and partially suppresses the duration of cortical epileptic afterdischarges.
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Nicotine has been repeatedly reported as substance possessing neuroprotective properties. This study focused on the possible beneficial effects of nicotine against the high-altitude hypoxia (9000 m for one hour). 15 min prior to hypoxia exposition rats (12- and 35-day-old) were treated with
Impaired cardiac function during postnatal hypoxia in rats exposed to nicotine prenatally: implications for perinatal morbidity and mortality, and for sudden infant death syndrome.
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Maternal smoking correlates highly with parturitional/neonatal death including SIDS; nicotine exposure of fetal rats reproduces the increased mortality when animals are tested postnatally with hypoxia. In the current study, pregnant rats received nicotine infusions simulating smokers' plasma
Postnatal nicotine and/or intermittent hypercapnic hypoxia effects on apoptotic markers in the developing piglet brainstem medulla.
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The most important risk factors currently identified for the sudden infant death syndrome (SIDS) are prone sleeping and cigarette smoke exposure. In this study, we investigated the neuropathological sequelae of these risk factors by exposing piglets to intermittent hypercapnic-hypoxia (IHH) and/or
Hypoxia recruits a respiratory-related excitatory pathway to brainstem premotor cardiac vagal neurons in animals exposed to prenatal nicotine.
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The most ubiquitous form of arrhythmia is respiratory sinus arrhythmia in which the heart beat slows during expiration and heart rate increases during inspiration. Whereas respiratory sinus arrhythmia benefits pulmonary gas exchange respiratory dysfunction presents a major challenge to the
Effect of nicotine exposure on postnatal ventilatory responses to hypoxia and hypercapnia.
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The risk of SIDS is increased up to fourfold by maternal smoking, by an unknown mechanism. We tested the hypothesis that prenatal nicotine exposure can cause abnormal postnatal development of breathing control. Osmotic minipumps were implanted into pregnant rats to deliver either nicotine bitartrate
Nicotine inhibits hypoxia- and arachidonate-induced release of prostacyclin-like activity in rabbit hearts.
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1 Rabbit hearts were perfused by the Langendorff technique and the interstitial effluent content of platelet anti-aggregatory activity (prostacyclin-like activity) was assayed at regular intervals. 2 Perfusion was performed with a solution containing 5% CO2 in O2. At regular intervals it was changed
Orexin receptors in the developing piglet hypothalamus, and effects of nicotine and intermittent hypercapnic hypoxia exposures.
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Orexin and its receptors (OxR1 and OxR2) play a significant role in arousal and sleep regulation. Using developing piglets, we aimed to determine the effects of nicotine and Intermittent Hypercapnic Hypoxia (IHH), alone or in combination, on orexin receptor expression in the hypothalamus. Four
Changes in orexinergic immunoreactivity of the piglet hypothalamus and pons after exposure to chronic postnatal nicotine and intermittent hypercapnic hypoxia.
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We recently showed that orexin expression in sudden infant death syndrome (SIDS) infants was reduced by 21% in the hypothalamus and by 40-50% in the pons as compared with controls. Orexin maintains wakefulness/sleeping states, arousal, and rapid eye movement sleep, abnormalities of which have been
Newborn piglets exposed to hypoxia after nicotine or saline pretreatment: long-term effects on brain and heart.
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OBJECTIVE
We wished to assess the effect of global hypoxia and the effect of nicotine pretreatment on the brain and heart of newborn pigs. Hypothesising that nicotine might give a better outcome because of its anti-apoptotic and anti-inflammatory effects.
METHODS
Twenty-two anaesthetised piglets
Protective effect of nicotine through nicotinic acetylcholine receptor alpha 7 on hypoxia-induced membrane disintegration and DNA fragmentation of cultured PC12 cells.
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To investigate the effect of nicotine on hypoxic neuronal damage, cultured PC12 cells were exposed to hypoxia for 9 h and then reoxygenated for 72 h. The cells were stained by propidium iodide (PI), a marker of cell membrane disintegration and the TUNEL method, which indicates DNA fragmentation. In
Hypoxia and nicotine effects on Pituitary adenylate cyclase activating polypeptide (PACAP) and its receptor 1 (PAC1) in the developing piglet brainstem.
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Pituitary adenylate cyclase activating polypeptide (PACAP) and its cognate receptor 1 (PAC1), have been implicated in the pathophysiology of the Sudden Infant Death Syndrome (SIDS). Two main risk factors for SIDS are prone sleeping and cigarette smoke exposure. Using piglet models of these risk
Chronic nicotine induces hypoxia inducible factor-2α in perinatal rat adrenal chromaffin cells: role in transcriptional upregulation of KATP channel subunit Kir6.2.
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Fetal nicotine exposure causes impaired adrenal catecholamine secretion and increased neonatal mortality during acute hypoxic challenges. Both effects are attributable to upregulation of ATP-sensitive K(+) channels (K(ATP) channels) and can be rescued by pretreatment with the blocker, glibenclamide.
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