Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
PMID:Plasma dopamine, norepinephrine, epinephrine and DOPAC levels in preterm infants prior to and immediately after a sleep ventilation hypercarbia test. 175 Mar 32

There is a wide variability in the therapeutic responsiveness to exogenous surfactant, a drug that has become generally available for the treatment of lung immaturity and respiratory distress syndrome. Recent studies have demonstrated evidence that therapies decreasing lung edema improve the effectiveness of surfactant substitution. In addition, exogenous surfactant may acutely decrease pulmonary perfusion since the airway pressures are effectively transmitted to airspaces, compressing alveolar capillaries, especially in hypovolemia. Therapies aimed at decreasing lung edema, improving cardiac output, and stepwise weaning from oxygen and ventilatory pressures are cornerstones in the successful management of patients undergoing surfactant therapy.
 ...
PMID:Factors affecting surfactant responsiveness. 177 26

Thirty-four long-term survivors of a five-year period (1977-1981) weighing 1000 g or less at birth were followed-up at 8-11 years of age. Fifty per cent of this population was qualified as normal. The great majority of the children (24) attended normal school but 7 (20.6%) with need of special help. There were only three children (8.8%) with severe functional impairment. The rate of survival was 30% at the Neonatal Intensive Care Unit of the Department of Pediatrics, University Medical School, Debrecen at that period of time. The authors analyze in detail the connections of the perinatal events and the outcome. While survival was influenced primarily by hemorrhagic complications beyond immaturity, the long-term prognosis depended on birth asphyxia, recurrent apneic spells and requirements for oxygen therapy.
 ...
PMID:[Follow up of extremely low birth weight infants at the age of 8-11 years (late prognosis of perinatal factors)]. 187 Aug 49

In its normal circulatory environment, the fetal left ventricle can maximally increase output less than 2-fold, in contrast to the nearly 3-fold increase that occurs at birth. Several studies have attributed this finding to fetal myocardial "immaturity," and speculated that there is a rapid maturation of the myocardium in the perinatal period. We investigated the importance of the circulatory environment itself, rather than myocardial immaturity, by measuring left ventricular output (LVO) during in utero oxygen ventilation and isoproterenol infusion. We studied seven near-term fetal sheep greater than or equal to 2 d after placement of intravascular catheters, an endotracheal tube, and an electromagnetic flow transducer around the ascending aorta. We measured hemodynamic variables in the presence and absence of all combinations of oxygen ventilation, isoproterenol infusion, and volume infusion. Baseline LVO was normal (133 +/- 27 mL.kg-1.min-1). Individually, oxygen ventilation (136 +/- 11 mL.kg-1.min-1, p less than 0.001) and isoproterenol (48 +/- 11 mL.kg-1.min-1, p less than 0.05) increased LVO significantly; volume infusion did not. Their cumulative effect increased LVO nearly 3-fold (to 387 +/- 98 mL.kg-1.min-1), similar to levels seen in the newborn lamb. Mean left atrial pressure increased above right during oxygen ventilation (from 0.05 +/- 0.54 kPa to 0.82 +/- 0.39 kPa, p less than or equal to 0.0001). We conclude that the previously observed limitation in maximal LVO in the near-term fetus is primarily caused by its circulatory environment rather than relative myocardial immaturity, and speculate that a prominent Starling response is uncovered by decreases in left ventricular afterload and right ventricular constraint.
 ...
PMID:In utero ventilation augments the left ventricular response to isoproterenol and volume loading in fetal sheep. 189 50

The premature baboon delivered by hysterotomy at 140 +/- 2 days (75%) gestation develops hyaline membrane disease (HMD) and left-to-right (L-R) shunting through the patent ductus arteriosus (PDA). To characterize hemodynamic changes that follow premature delivery, we measured systemic and organ blood flow, oxygen transport, and systemic vascular resistance over the first 96 h of life. We compared these measurements with those from more mature animals of the same species. Radiolabeled microspheres were used to measure organ blood flow (in ml.min-1.g-1) at 3 (n = 18), 23 (n = 17), and 96 h (n = 4) in the premature animals, and at 13 +/- 4 mo in the older animals (n = 5). Premature animals demonstrated over the first 96 h of life significant hemodynamic changes that included decreased systemic vascular resistance (P less than 0.001), increased systemic (P less than 0.05), intestinal (P less than 0.05), and hepatic blood flow (P less than 0.05), as well as resolution of L-R PDA shunting. These 96-h values were similar to those of the more mature infant baboons. Blood flow and oxygen transport to the kidneys and cerebrum did not significantly increase over the first 96 h in premature baboons and were significantly less than those of 13-mo-old animals (P less than 0.01, both). We speculate that low renal and cerebral blood flow in the 140-day premature baboon are manifestations of multisystem immaturity and, as such, may represent persistent physiological disturbances that are distinct from the severity of underlying lung disease in HMD.
 ...
PMID:Circulatory changes following premature delivery in a baboon model of hyaline membrane disease. 192 96

Erythrocytosis and microcytosis have been described in strains of genetically hypertensive rats and in essentially hypertensive humans. Published discussion of these phenomena has centered around their relationship to observed alterations in ionic transport and the pathogenesis of hypertension. In presenting data for another strain of spontaneously hypertensive rats in which these findings are exhibited, we note that erythroid cell size decreases concurrently with the increase in cell numbers so that the hematocrit and the mean corpuscular hemoglobin concentration remain constant. Data from the literature support the hypothesis that erythroid cell size is inversely proportional to cell count in a large number of species. Erythrocytosis, as it develops in the neonatal rat, is a consequence of the marked immaturity of this species at birth. Erythrocytosis in the spontaneously hypertensive rat is not due to a difference in the affinity of its hemoglobin for oxygen or to significant tissue anorexia. Microcytosis in the spontaneously hypertensive rat is the consequence of a continuation of the linear volume decrease with age of its erythroid cells seen in the normotensive animals and may be accounted for by the production of smaller cells with concomitant regulation of individual cell volume.
 ...
PMID:Inverse changes in erythroid cell volume and number regulate the hematocrit in newborn genetically hypertensive rats. 194 11

Previous study has shown that midorganogenesis-stage rat embryos exposed to strong redox cyclers under moderate hypoxia in vitro develop severe necrotic defects on the right side. Similar effects can be produced by exposure to severe hypoxia alone. Studies presented here indicate that exposure to severe but survivable hyperoxia induces comparable necrotic degeneration on the left sides of all embryos. We hypothesize that the basis of these axially asymmetric defects is relatively precocious mitochondrial maturity on the left side of the embryo. In order to investigate this hypothesis, we compared mitochondrial oxygen utilization (NADH oxidase activities) on either side of rat embryos between days 11 and 14 of gestation. Activities were consistently higher on the left side during this period and significantly higher on day 11. We also found that the asymmetric embryotoxicity induced by niridazole, a strong redox cycler, could be attenuated by prior culture under hyperoxic conditions. We propose that mitochondrial immaturity on the right results in inadequate energy generation under hypoxic conditions, either directly or as a result of redox cycling. On the other hand, necrosis associated with hyperoxic conditions results from "leakage" of superoxide from functionally mature mitochondria on the left side.
 ...
PMID:Asymmetric development of mitochondrial activity in rat embryos as a determinant of the defect patterns induced by exposure to hypoxia, hyperoxia, and redox cyclers in vitro. 194 69

Retinopathy of prematurity has reappeared in the neonatal nursery after largely disappearing 35 years ago. The major factor in its reemergence is the progressive improvement in neonatal care, resulting in salvage of infants who formerly would have been lost. Oxygen is now recognized to be but one of many interacting factors in the development of retinopathy of prematurity, with extreme immaturity being the primary factor. Methods of examination, classification and treatment of retinopathy of prematurity are discussed.
 ...
PMID:Retinopathy of prematurity. 219 77

Identification of a suitable animal model is essential for the continued study of retinopathy of prematurity (ROP). Since 1984 we have used the newborn rat for the study of oxygen-induced retinopathy (OIR). The rat retina is highly immature at birth. Like those of humans, the retinal vessels arise from mesenchymal precursors, but contrary to that which occurs in humans, canalization of the rats inner retinal vessels is not related to the presence of cystoid spaces. In addition, only immature Stage I photoreceptors are present around the optic disk at birth. This extreme immaturity makes the rat retina highly susceptible to direct damage from oxygen. Oxygen-induced retinopathy can be produced by exposing the newborn rat to 80% oxygen for the first 7-10 days of life. We have demonstrated that OIR does not develop when oxygen is administered under conditions of moderate hyperbarism (+1.8 atm). It is possible that hyperbarism exerts a protective effect on the immature retinal vessels by inducing a vasoconstrictive response which reduces the amount of oxygen transported from the choroid to the inner retina during hypoxia. I recently hypothesized that this vasoconstriction might also affect the ciliary body, thus reducing the quality of aqueous produced, and we are currently studying the relationship between development of the immature retinal vessels in the rat and production and drainage of the aqueous. The question we are attempting to answer is whether a condition of relatively increased intraocular pressure is capable of promoting the development of OIR.
 ...
PMID:Oxygen-induced retinopathy in the rat model. 220 74

Retinopathy of prematurity (ROP) has increased in the United States in the past decade. Its resurgence has been attributed to advances in medical care which have increased the survival of infants less than 1000 g. Retinal immaturity and exposure to supplementary oxygen are generally accepted as the principal factors associated with ROP, however precocious exposure of the immature retina to light may also contribute. The preterm infant is routinely exposed for the duration of hospital stay to bright continuous light at levels which produce retinal damage in animals. A recent study has provided evidence implicating light in ROP. Preterm infants for whom the light levels were reduced had a lower incidence of ROP, compared to a similar group of preterms exposed to standard levels of nursery light. Given the problems of a non-randomized design, the results must be considered preliminary; however the findings are substantiated by parallel results in both hospitals studied and by an effect of exposure to light within the treatment group. Speculations regarding the mechanisms of light as a contributor to ROP include: alterations of retinal metabolism, cellular damage by phototoxicity, and the generation of free radicals. Mechanisms of phototoxicity are compatible with theories of oxygen toxicity. Light may not be necessary for ROP to occur, but it may increase the risk.
 ...
PMID:Light and the developing retina. 220 77


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>