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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postnatal maturation and the adaptational ability of the sympathoadrenal system has been investigated in preterm neonates (n = 8), and in sick preterm neonates with respiratory disorders (n = 10). Plasma levels of dopamine (DA), norepinephrine (NE), epinephrine (E) and 3-4 dihydroxyphenylacetic acid (DOPAC) were evaluated at rest during the first month of life, and following an inhalation of a 5% carbon dioxide-21% oxygen mixture for 10 min. During the first month of life the sick preterm neonates exhibited similar NE, E, and DOPAC plasma levels but higher DA amounts than healthy infants. Plasma DA levels were inversely correlated with the transcutaneous oxygen tension (r = -0.636) indicating that hypoxemia was able to enhance the release of DA. Immediately following the hypercarbia test, there were no significant changes of plasma catecholamine levels in the sick preterms, but there was a significant increase of E plasma levels (+140%, p less than 0.05) and a moderate elevation of NE and DA amounts in the healthy preterms. It is concluded that preterm neonates who have had respiratory disorders did not exhibit an immaturity of the sympathoadrenal system at rest, but had a defect in the release of E following hypercarbia exposure, which may be secondary to an alteration in chemoreceptor function and/or reduced catecholamine stores.
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PMID:Plasma dopamine, norepinephrine, epinephrine and DOPAC levels in preterm infants prior to and immediately after a sleep ventilation hypercarbia test. 175 Mar 32

Intraventricular hemorrhage (IVH) in preterm infants is well known to be associated with the high morbidity and mortality of this group. Previous studies have suggested altered cerebral blood flow (CBF) as an important pathologic factor. We measured the CBF in near-term rabbit fetuses using the hydrogen clearance technique. The local CBF of the rabbit fetuses was significantly low compared with that of the maternal rabbits. The response of CBF to changes in PaCO2 was observed in rabbit fetuses. The CO2 reactivity index of the fetal rabbit was lower than that of the maternal rabbit. This low CO2 reactivity might reflect the immaturity of the fetal brain and its low CBF. We were unable to monitor the fetal blood pressure, but the fetal CBF remained stable when the maternal blood pressure was altered. It is well known that IVH in preterm infants originates from the subependymal germinal matrix and that this has many fragile vessels. Our observation suggests that even a small increase of CBF during hypercapnia might have a large effect towards producing hemorrhage.
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PMID:CO2 reactivity and autoregulation in fetal brain. 176 8

This study was aimed at determining the role of carotid bodies in the initiation and maintenance of oral breathing during nasal obstruction. We have previously shown in sheep that oral breathing during nasal obstruction was less effective in the neonate than in older lambs or adults. We considered it possible that the reduced response of the neonate was due to immaturity of carotid body chemoreceptors. Respiratory and blood gas responses to nasal obstruction were determined in 5 neonatal lambs, 6 older lambs and 6 adult ewes before and after surgically denervating the carotid bodies. Denervations were performed at 4.2 +/- 0.9 days after birth in the neonatal lambs and at 41.5 +/- 2.5 days in the older lambs. Carotid body denervation led to hypoxia, hypercapnia and acidaemia in lambs and ewes during unobstructed nasal breathing, and, in response to nasal obstruction, delayed the onset of oral breathing so that it occurred at a greater degree of hypoxia. Following carotid body denervation the degree of hypercapnia and acidaemia during nasal obstruction was greater in lambs than in ewes. We conclude that the carotid bodies in lambs and ewes play an important role in the regulation of normal blood gases and pH, and in the establishment and effectiveness of oral breathing during nasal obstruction.
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PMID:The role of carotid bodies in the establishment of oral breathing during nasal obstruction in lambs and ewes. 211 63

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.
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PMID:Bicarbonate reabsorption by the kidney of the newborn rabbit. 291 64

The aims of this study were to compare the ability of awake newborn lambs and adult sheep to breathe orally when the nasal route was blocked and to determine the means by which it was accomplished. Chronic EMG electrodes (diaphragm, genioglossus, geniohyoid, posterior crico-arytenoid, digastric, thyroarytenoid) and fibre-optic catheters were implanted in 10 lambs and 4 ewes. Before each study soft tubes were fixed into the nostrils allowing rapid blockade of the nasal ventilatory pathway. During nasal blockade inspiratory upper airway dilator EMG activity increased. SaO2 fell until mouth opening occurred, then returned to near control values; oral breathing then ceased leading to desaturation again. In lambs and ewes there was significant hypoxia, hypercapnia and acidaemia. In lambs 2-14 days old, PO2 and pH fell to lower levels than in older lambs (15-30 days) or ewes and PCO2 rose more. In lambs PCO2 gradually increased during the period of obstruction. We conclude that maintenance of blood gas homeostasis in newborn lambs is more severely impaired by nasal obstruction than in older lambs or ewes, possibly due to an immaturity of neural mechanisms controlling the creation of an oral airway.
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PMID:Respiratory and upper airway responses to nasal obstruction in awake lambs and ewes. 311 Aug 90

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

1. Low birthweight is now recognized as an important risk factor for early postnatal respiratory illness and it is becoming evident that low birthweight can increase the risk for airway dysfunction in children and adults. Our studies have been aimed at determining how low birthweight, resulting from intra-uterine growth restriction (IUGR), affects the control of breathing and the structural and functional development of the lung. 2. We have measured ventilatory responsiveness to progressive hypoxia and progressive hypercapnia during the first weeks after birth in postnatal lambs in which IUGR was induced by chronic placental insufficiency. It was found that the postnatal increase in ventilatory sensitivity to hypoxia observed in control lambs was diminished in low birthweight lambs; in contrast, the sensitivity to hypercapnia was not affected. In other studies, we found that IUGR caused by maternal anaemia led to elevated CO2 levels during sleep and wakefulness. 3. Our findings suggest that the prenatal development of the brain-stem or respiratory chemoreceptors may be affected by intra-uterine factors associated with IUGR, such as foetal hypoxaemia or hypoglycaemia. It is also possible that the structure of respiratory muscles and, hence, their ability to maintain a high level of ventilation may be affected by IUGR. 4. Recently, we studied the influence of IUGR on foetal lung development, in particular its effects on foetal lung liquid, a major determinant of lung growth, as well as alveolar structure and pulmonary surfactant. Lung liquid secretion and volume, in relation to bodyweight, were unaffected; however, there was evidence of structural and functional immaturity in the lungs. In foetuses exposed to IUGR, the air-blood barrier was thicker and, after birth, the diffusing capacity of the lungs for carbon monoxide was lower. In contrast, surfactant protein gene expression was enhanced, particularly in foetuses with high levels of circulating cortisol. 5. Further studies are needed to characterize the effects of specific types of prenatal compromise on postnatal control of ventilation and lung function, to determine mechanisms underlying these effects and to determine the capacity for postnatal recovery.
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PMID:Effects of intra-uterine growth restriction on the control of breathing and lung development after birth. 1069 39

Carbon dioxide (CO(2)) plays important roles in regulating both respiratory drive and cerebral blood flow. These effects are mediated, in part, by activity of the sympathetic nervous system. We hypothesized that the presence of acute life-threatening events or apnea in term or preterm infants, respectively, would serve as a marker for immaturity of cerebral autonomic innervation and that such infants would display a reduced cerebral vascular response to elevated pCO(2). Therefore, we evaluated the cerebral vascular response during CO(2) challenge tests in groups of term and preterm infants with primary apnea. In term infants (39 +/- 2 weeks gestation) with acute life-threatening events, elevated pCO(2) was accompanied by decreasing pulsatility index and increasing mean anterior cerebral blood flow velocity. However, in preterm infants (29 +/- 2 weeks' gestation) with apnea, pulsatility index and anterior cerebral artery flow velocity did not significantly change in response to CO(2) supplementation. We conclude that preterm, but not term, infants with apnea exhibit impaired vascular responses to hypercarbia.
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PMID:Cerebral vascular responses to changes in carbon dioxide tension in term and preterm infants with apnea. 1290 45

This study was designed to examine the ventilatory performance and the lung histopathology of cystic fibrosis knockout mice (Cftr-/-) compared with heterozygous (Cftr+/-) or wild-type (Cftr+/+) littermates. Ventilation was recorded in conscious animals using whole-body plethysmography. Tidal volume (VT), respiratory frequency (f), and minute ventilation (VE) were measured during air breathing and in response to various levels of hypercapnia (2, 4, 6, or 8% CO2) or hypoxia (14, 12, 10, or 8% O2). The results for Cftr+/- and Cftr+/+ were pooled into one control group because they did not differ. In air and in response to hypercapnia, VE, VT, and f were similar in Cftr-/- mice and in controls. During graded hypoxia, VE was decreased in Cftr-/- mice at 10 and 8% O2 because of a lower f. Histology showed neither inflammation nor obstruction of airways in Cftr-/- mice. Morphometric analysis showed alveolar dilation as a result of either distension or impaired development. In conclusion, cystic fibrosis knockout mice have normal baseline breathing and ventilatory response to hypercapnia but a decreased ventilatory response to severe hypoxia. This latter result associated with the morphometric analysis suggests that Cftr-/- mice may exhibit immaturity of the respiratory system.
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PMID:Ventilatory responses to hypercapnia and hypoxia in conscious cystic fibrosis knockout mice Cftr-/-. 1476 16

Respiratory control in the fetus and neonate is quite immature when compared to that of adults. This immaturity involves all facets of respiration including respiratory responses to hypoxia, hypercapnia, an exaggerated apnoeic response to laryngeal stimulation and immature responses to activation of pulmonary afferents. The net result of this immaturity of breathing responses is the vulnerability of neonates and especially preterm infants to apnoea and respiratory pauses. The mechanisms behind immature control of breathing are not fully understood, but seem to originate from a predominance of inhibitory input early in life on respiratory centres. The relative contribution of up-regulation of inhibitory pathways versus down-regulation of excitatory ones is not clear. Multiple neurotransmitters have been implicated in the regulation of breathing in mammals and some of them are discussed in this chapter.
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PMID:Maturation of respiratory reflex responses in the fetus and neonate. 1505 Feb 10


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