Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0242706 (hyperoxia)
5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

In order to determine indicators for the risk of SIDS (sudden infant death syndrome) the respiratory responses of babies (age 1 to 5 months) during sleep to various gas mixtures was examined. Using a face mask combined with a pneumotachograph in all cases a marked increase of the ventilation was found, when the babies were exposed to pure oxygen. Furthermore, the response of the babies to the exposure to mild hypoxia was tested. In 24 out of 36 babies a ventilatory depression was observed which sometimes was coupled with periodic or arrhythmic ventilation. These paradox reactions--depression by mild hypoxia and stimulation by hyperoxia--might be related to a possible circulus vitiosus in the pathogenesis of SIDS.
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PMID:[Paradoxical ventilatory response of babies to pure oxygen (author's transl)]. 676 98

Decreased ability to generate a hyperventilatory response to hypoxemia is believed to be an important mechanism in the pathophysiology of sudden infant death syndrome, and maternal smoking is a leading risk factor. To investigate whether there may be a link between these two observations, we studied five lambs at mean ages of 7, 17, and 27 d to determine the effects of an i.v. infusion of nicotine (0.5 microgram/kg/min) on ventilation when peripheral chemoreceptor activity was stimulated by hypoxia (0.1 FiO2) or briefly inhibited by hyperoxia. Ventilatory measurements were performed using a computer-aided occlusion valve device which permitted breath-by-breath determinations of inspiratory occlusion pressures (P0.1) and minute ventilation. Nicotine attenuated the early ventilatory response to hypoxia (min 1, 2, and 3 of the test) by 8, 26, and 37%, respectively, at the age of 7 d (analysis of variance overall, p < 0.05), by 23%, 23 and 37% at 17 d (p = NS) and by 40, 45, and 37% at 27 d (p < 0.05). The decrease in ventilation in response to hyperoxia during the control study without nicotine was 18, 35, and 34% at 7, 17, and 27 d, respectively. Nicotine caused a greater decrease in the response: 31, 45, and 46%, respectively, (p < 0.05 at 27 d). The paradoxical effects of nicotine, attenuation of the ventilatory response to hypoxia and augmentation of the response to hyperoxia, suggest that nicotine altered peripheral chemoreceptor oxygen sensitivity and most likely also affected central processing of the chemoreceptor input.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nicotine attenuates the ventilatory response to hypoxia in the developing lamb. 760 86

Ten preterm infants with chronic lung disease (CLD) and undeveloped peripheral chemoreceptor function, described as ventilatory response to hyperoxia, were investigated, according to an individual protocol. Each infant was followed up until the response to hyperoxic inhalation had been observed on two occasions. Each examination consisted of overnight recording of saturation, testing of lung compliance and airway resistance, and the hyperoxic test. The hyperoxic response appeared at a mean postnatal age of 14 weeks (range 9-33 weeks). This response, which was independent of the infant's lung mechanics, appeared much later in infants with the severe form of CLD. As undeveloped peripheral chemoreceptor function has been suggested to be a key factor in sudden infant death syndrome (SIDS), the delayed development of their chemosensitivity leaves some infants with CLD unprotected against hypoxia at the age at which the risk for SIDS is highest.
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PMID:Development of peripheral chemoreceptor function in infants with chronic lung disease and initially lacking hyperoxic response. 879 49

Because smoking during pregnancy is a major risk factor for late fetal death and the sudden infant death syndrome, we investigated cardiorespiratory defense mechanisms to hypoxia in 7 prenatally nicotine-exposed (N) lambs (approximate maternal dose: 0.5 mg/kg/day) and 11 control (C) lambs all at an average age of 5 days. The ventilatory response to 10% oxygen (hyperpnea) was significantly attenuated during quiet sleep in N lambs compared with C lambs and in N lambs aroused from sleep later compared with C lambs (161 +/- 90 versus 75 +/- 66 seconds, p < 0.05). The ventilatory response to hypoxia was similar in the two groups during wakefulness (W), whereas the heart rate response (tachycardia) was significantly lower in N lambs compared with C lambs during both activity states. The ventilatory response to hyperoxia was significantly lower in N lambs compared with C lambs during both activity states. Transition from W to quiet sleep was associated with a significant decrease in ventilation in C lambs but not in N lambs. In conclusion, prenatal nicotine exposure, at a dose comparable with moderate smoking, blunts major elements of the cardiorespiratory defense to hypoxia, i.e., the heart rate and ventilatory and arousal responses, and abolishes the normal decrease in ventilation during sleep compared with W.
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PMID:Prenatal nicotine exposure blunts the cardiorespiratory response to hypoxia in lambs. 1247 Oct 66

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 detrimental. Nicotine interacts with endogenous acetylcholine receptors in the brain and lung, and developmental exposure produces structural changes as well as alterations in neuroregulation. Abnormalities have been described in sympathicovagal balance, arousal threshold and latency, breathing pattern at rest and apnea frequency, ventilatory response to hyperoxia or hypoxia, heart rate regulation and ability to autoresuscitate during severe hypoxia. This review discusses studies performed on infants of smoking mothers and nicotine-exposed animals yielding varying and sometimes inconsistent results that may be due to differences in experimental design, species and the dose of exposure. Taken together however, developmental nicotine exposure appears to induce vulnerability during hypoxia and a potential inability to survive severe asphyxia.
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PMID:Cardiorespiratory effects of nicotine exposure during development. 1597 Apr 70

The aim of the present paper is to briefly review the changes occurring in the nucleus tractus solitarii and carotid body in response to hypoxic and hyperoxic injuries. Selective alterations of dendrites and Fos-immunoreactivity of neurons have been observed in the subnucleus gelatinosus of the nucleus tractus solitarii of adult subjects dying after hypoxic-ischaemic injury. The selective vulnerability of this portion of the nucleus tractus solitarii may be explained mainly with reference to the vascularization of medullary tegmentum. In the carotid body, chronic hypoxia and hyperoxia cause a series of morphological, cellular and biochemical changes which may play a major role during the first postnatal period and may have implications in the pathogenesis of Sudden Infant Death Syndrome. Intermittent hypoxia may cause hypersensitivity of the carotid body, possibly increasing the risk of unstable respiration. Conversely, hyperoxia exposure has been reported to cause hyposensitivity and reduction in volume of the carotid body, possibly leading to ineffective response.
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PMID:Anatomical basis of hypoxic and hyperoxic injuries to the centres of cardiorespiratory regulation. 2107 89

The aim of the present study is to provide a review of cytochemical, clinical and experimental data indicating disruption of perinatal carotid body maturation as one of the possible mechanisms underlying SIDS pathogenesis. SIDS victims have been reported to show alterations in respiratory regulation which may partly be ascribed to peripheral arterial chemoreceptors. Carotid body findings in SIDS victims, although not entirely confirmed by other authors, have included reductions in glomic tissue volume and cytoplamic granules of type I cells, changes in cytological composition (higher percentages of progenitor and type II cells) and increases in dopamine and noradrenaline contents. Prematurity and environmental factors, such as exposure to tobacco smoke, substances of abuse, hyperoxia and continuous or intermittent hypoxia, increase the risk of SIDS and are known to affect carotid body functional and structural maturation adversely, supporting a role for peripheral arterial chemoreceptors in SIDS.
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PMID:The carotid body in Sudden Infant Death Syndrome. 2261 76

We have identified a critical period of respiratory development in rats at postnatal days P12-13, when inhibitory influence dominates and when the response to hypoxia is at its weakest. This critical period has significant implications for Sudden Infant Death Syndrome (SIDS), the cause of which remains elusive. One of the known risk factors for SIDS is prematurity. A common intervention used in premature infants is hyperoxic therapy, which, if prolonged, can alter the ventilatory response to hypoxia and induce sustained inhibition of lung alveolar growth and pulmonary remodeling. The goal of this study was to test our hypothesis that neonatal hyperoxia from postnatal day (P) 0 to P10 in rat pups perturbs the critical period by altering the normal progression of neurochemical development in brain stem respiratory-related nuclei. An in-depth, semiquantitative immunohistochemical study was undertaken at P10 (immediately after hyperoxia and before the critical period), P12 (during the critical period), P14 (immediately after the critical period), and P17 (a week after the cessation of hyperoxia). In agreement with our previous findings, levels of cytochrome oxidase, brain-derived neurotrophic factor (BDNF), TrkB (BDNF receptor), and several serotonergic proteins (5-HT_1A and _2A receptors, 5-HT synthesizing enzyme tryptophan hydroxylase [TPH], and serotonin transporter [SERT]) all fell in several brain stem respiratory-related nuclei during the critical period (P12) in control animals. However, in hyperoxic animals, these neurochemicals exhibited a significant fall at P14 instead. Thus, neonatal hyperoxia delayed but did not eliminate the critical period of postnatal development in multiple brain stem respiratory-related nuclei, with little effect on the nonrespiratory cuneate nucleus.
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PMID:Effects of neonatal hyperoxia on the critical period of postnatal development of neurochemical expressions in brain stem respiratory-related nuclei in the rat. 2951 54

Twenty-five years ago, Filiano and Kinney (1994) proposed that a critical period of postnatal development constitutes one of the three risk factors for sudden infant death syndrome (SIDS). The underlying mechanism was poorly understood. In the last 17 years, much has been uncovered on this period in the rat. Against several expected trends of development, abrupt neurochemical, metabolic, ventilatory, and electrophysiological changes occur in the respiratory system at P12-13. This results in a transient synaptic imbalance with suppressed excitation and enhanced inhibition, and the response to acute hypoxia is the weakest at this time, both at the cellular and system's levels. The basis for the synaptic imbalance is likely to be contributed by a reduced expression of brain-derived neurotrophic factor (BDNF) and its TrkB receptors in multiple brain stem respiratory-related nuclei during the critical period. Exogenous BDNF or a TrkB agonist partially reverses the synaptic imbalance, whereas a TrkB antagonist accentuates the imbalance. A transient down-regulation of pituitary adenylate cyclase-activating polypeptide (PACAP) at P12 in respiratory-related nuclei also contributes to the vulnerability of this period. Carotid body denervation during this time or perinatal hyperoxia merely delays and sometimes prolongs, but not eliminate the critical period. The rationale for the necessity of the critical period in postnatal development is discussed.
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PMID:Mechanisms underlying a critical period of respiratory development in the rat. 3099 61


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