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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of peripheral arterial chemodernervation on laryngeal reflex-induced apnea were studied in 18 piglets of either sex varying in age from 4 to 63 days. The distal trachea was cannulated with a cuffed endotracheal tube to secure a free airway and permit ventilatory measurements with a pneumotachograph. The proximal trachea was used to introduce fluids into the larynx. Water elicited apnea, bradycardia, and arterial hypertension, whereas saline caused only transient disturbances. Electrical stimulation of the superior laryngeal nerves reproduced, and conduction anesthesia ablated, the effects of water in the larynx. Carotid body contribution to respiratory drive was assessed by the ventilatory responses to increased (100%) and decreased (10%) anbient oxygen concentration. These indicated significant peripheral chemoreceptor ventilatory activity from birth with little further change in the neonatal period. Ventilatory responses to oxygen were ablated by carotid chemodenervation, but there was no change in the duration of laryngeal reflex apnea. We conclude that attenuation of laryngeal-induced apnea during postnatal development is independent of peripheral chemoreceptor activity. Our findings may have relevance to the clinical problem of sudden infant death syndrome, in which carotid body abnormalities have recently been described.
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PMID:Laryngeal reflex apnea in the chemodenervated newborn piglet. 46 79

Prenatal cocaine use has become an increasingly important public health problem in the last decade. Interpretation of epidemiologic studies designed to assess the association between cocaine use and adverse pregnancy outcomes is limited by inaccurate measurement of cocaine use, misclassification of users as non-users, confounding by socioeconomic factors, and reporting bias. Studies have consistently documented placental abruption as a maternal reproductive risk associated with cocaine use. Although suggested, less evidence is available to link cocaine use with premature rupture of membranes, spontaneous abortion, pregnancy-induced hypertension, precipitate delivery, or fetal death. Infant outcomes consistently associated with prenatal cocaine use include decreased birth weight, prematurity, and decreased fetal growth. Data on the relationship between prenatal cocaine use and congenital anomalies are limited, but one large retrospective study has documented an association between maternal cocaine use and congenital abnormalities of the urinary tract. Evidence linking prenatal cocaine use and an increased incidence of perinatal cerebral infarction or sudden infant death syndrome is lacking. Future studies should focus on the effect of maternal cocaine use on pregnancy outcome in diverse socioeconomic groups, longitudinal follow-up of exposed children, and the relationship between cocaine use and maternal behaviors that may affect access to prenatal care.
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PMID:Risks associated with cocaine use during pregnancy. 156 65

Autonomic nervous system abnormalities have been implicated in infants dying of or considered at high risk of sudden infant death syndrome (SIDS). In a rat model, norepinephrine (0.02 mg/kg) caused systemic hypertension and numerous pulmonary petechiae, the latter a common finding in SIDS. Petechiae were not seen below the diaphragm. The animals were killed by tracheal occlusion 5 min after the intravenous administration of norepinephrine. The number of pulmonary petechiae was greatly reduced by alpha-adrenergic blockade (phentolamine) and dopaminergic blockade (haloperidol) but not by beta-adrenergic blockade (timolol). A significantly greater reduction of peak mean systemic arterial pressure occurred after alpha-adrenergic blockade than with other blocking agents. It is conceivable that hypoxia-induced endogenous catecholamine release contributes to the pathogenesis of pulmonary petechiae found at necropsy of SIDS victims.
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PMID:Norepinephrine-induced pulmonary petechiae in the rat: an experimental model with potential implications for sudden infant death syndrome. 654 10

As should be evident from the case reports, epidemiology studies, and animal data, the primary mode of cocaine action is vasoconstriction, whether it occurs on the maternal side or the fetal side of the placenta. Attempts to characterize the fetal effects of cocaine exposure during pregnancy in order to formulate a "fetal cocaine syndrome" has revealed a wide spectrum of fetal effects. Therefore, a well-defined "fetal cocaine syndrome" does not exist. In fact, most fetal defects may be related to vasoconstriction, hypertension, and infarcts at any time during gestation and in any structure. Even the issues of SIDS and seizures may be the result of clinically undetectable vasospasm or hemorrhages. Traditional dogma dictates that a teratogen interferes with normal development of a structure such that the structure is missing, malformed, or dysfunctional. Moreover, since individual structures are formed at specific times during development, these structures are vulnerable to injury at these "time windows." Classical teratogens exert their damaging effects during the organogenesis period. For cocaine, however, exposure during any period in gestation may place any organ or structure at potential risk for damage. While repeated exposures during pregnancy may increase the risk of cocaine-induced damage, it appears that even a single exposure may produce infarction, edema, and tissue necrosis. The site of damage may be related to the tissue level of cocaine and the weakness of the blood vessels at that site. Subsequent loss of vascular supply and tissue necrosis produce fetal damage that is beyond capacity for repair.
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PMID:Maternal, placental, and fetal pathophysiology of cocaine exposure during pregnancy. 851 24

1. Nicotine is involved in many cardio-respiratory diseases, including hypertension and sudden infant death syndrome (SIDS), which is the most common cause of death in infants between 1 month and 1 year of age. While the aetiology of SIDS remains largely unknown, recent clinical studies suggest maternal cigarette smoking is a major risk factor in SIDS and an abnormality of cardio-respiratory control, particularly a centrally mediated slowing of the heart that precedes or accompanies apnoea, is involved. 2. Because the sites, mechanisms of action and diverse receptor types of nicotine within the central nervous system are controversial and poorly understood, in the present study we examined the effects of nicotine on specific brainstem neurons that control heart rate. Cardiac vagal neurons were identified in an in vitro slice preparation using a retrograde fluorescent tracer and were studied using both whole-cell and perforated patch-clamp electrophysiological techniques. 3. We have found there are different pre- and post-synaptic nicotinic receptors that have dramatic effects on glutamatergic neurotransmission as well as directly activating vagal cardio-inhibitory neurons.
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PMID:Nicotine excites cardiac vagal neurons via three sites of action. 967 23

Although peripheral cholinergic neurotransmission has long been known to play a pivotal role in the control of heart rate and blood pressure, recent evidence has suggested that central cholinergic mechanisms may be involved in the genesis of hypertension, anxiety, cardiorespiratory control, and, in particular, the respiratory modulation of heart rate. Yet, the sites, mechanisms, and receptor subtypes involved in the action of nicotine within the central nervous system are controversial. The present study demonstrates that nicotine has at least 3 sites of action to increase the activity of vagal cardiac neurons. Nicotine, but not muscarinic agonists, activates postsynaptic receptors and a depolarizing inward current in vagal cardiac neurons studied with the perforated patch-clamp technique in a visualized brain stem slice. In addition, nicotine acts at different presynaptic and postsynaptic sites to facilitate glutamatergic neurotransmission. Presynaptic nicotinic receptors increase the frequency of transmitter release and are sensitive to block by alpha-bungarotoxin. Nicotine also elicits a previously undescribed augmentation of postsynaptic non-NMDA currents. The presynaptic and postsynaptic receptors may prove to be future targets in the search for agonists to increase vagal cardiac activity and reduce the fatality associated with cardiac hyperexcitability and for antagonists to reduce cardiac vagal activity in pathological conditions associated with abnormally low heart rates and cardiac function such as sudden infant death syndrome.
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PMID:Nicotine enhances presynaptic and postsynaptic glutamatergic neurotransmission to activate cardiac parasympathetic neurons. 985 41

Several reflexes are initiated in the fetus and newborn when hypochloremic or strongly acidic solutions contact the epithelium that surrounds the entrance to the laryngeal airway. These reflexes, known collectively as the laryngeal chemoreflex (LCR), include startle, rapid swallowing, apnea, laryngeal constriction, hypertension, and bradycardia. Many studies have shown that prolonged apnea associated with the LCR may be life threatening and might conceivably be a cause of sudden infant death syndrome. This certainly may be true, but the concept of a lethal LCR paradoxically contrasts with the view that these several reflexes have an important airway-protective role. As the infant matures, rapid swallowing and apnea become much less pronounced, whereas cough and possibly laryngeal constriction become more prominent. This transformation is primarily related to central neural processing rather than to changes in the airway mucosal "water receptors" that initiate the reflex. The LCR develops in the fetus, in an all-aqueous environment, during a period in which aspiration of amniotic fluid poses a serious threat to life. This and other considerations suggest that the transformation in LCR responses from fetal to adult life can be viewed as functionally appropriate to their primary role in defending the airway from aspiration. The laryngeal "water receptors" that initiate the LCR in infants and adults alike appear to be the primary sensory mechanism for defending the airway from aspiration of liquids.
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PMID:Maturation and transformation of reflexes that protect the laryngeal airway from liquid aspiration from fetal to adult life. 1174 29

The negative effects of passive smoking on the health of the foetus or child continue to receive little attention, despite the large volume of research in this area. Passive smoking during pregnancy is associated with low birth weight, a reduction in head circumference at birth, and a far higher incidence of sudden infant death syndrome. Exposure to cigarette smoke also leads to a decreased lung function, an increased risk of severe infections, including respiratory syncytial virus bronchiolitis, meningococcal disease and middle ear infections. There is no association between passive smoking and the development of allergic asthma, but passive smoking does cause an increase in the prevalence of respiratory symptoms in children with or without asthma. Finally, there is a relation between passive smoking and behavioural disorders including attention deficit/hyperactivity disorder (ADHD). Passive smoking before birth seems even more harmful than after birth. A causal relationship is suggested in most studies, or has been proven by animal experiments. A decreased birth weight in general increases the risk of developing chronic diseases as an adult, such as hypertension, cardiovascular disease and type 2 diabetes mellitus. This extensive knowledge about the adverse health effects of smoke exposure in (unborn) children deserves greater attention in the counselling of pregnant women, and in anti-smoking campaigns.
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PMID:[Negative effects of passive smoking on the (unborn) child]. 1199 61

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

Respiratory network plasticity is a modification in respiratory control that persists longer than the stimuli that evoke it or that changes the behavior produced by the network. Different durations and patterns of hypoxia can induce different types of respiratory memories. Lateral pontine neurons are required for decreases in respiratory frequency that follow brief hypoxia. Changes in synchrony and firing rates of ventrolateral and midline medullary neurons may contribute to the long-term facilitation of breathing after brief intermittent hypoxia. Long-term changes in central respiratory motor control may occur after spinal cord injury, and the brain stem network implicated in the production of the respiratory rhythm could be reconfigured to produce the cough motor pattern. Preliminary analysis suggests that elements of brain stem respiratory neural networks respond differently to hypoxia and hypercapnia and interact with areas involved in cardiovascular control. Plasticity or alterations in these networks may contribute to the chronic upregulation of sympathetic nerve activity and hypertension in sleep apnea syndrome and may also be involved in sudden infant death syndrome.
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PMID:Invited review: Neural network plasticity in respiratory control. 1257 Nov 45


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