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Neonatal diseases II
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Brian P. Hackett, Jeffrey Dawson, Akshaya Vachharajani, Barbara Warner, F. Sessions Cole
In 1959, Mary Ellen Avery and Jere Mead described the relationship between preterm birth, lung surface tension, and RDS (21). Since that time, understanding the biology of pulmonary surfactant and its role in preterm respiratory distress has been one of the triumphs of newborn medicine. This understanding has led to the use of exogenous surfactant replacement as a primary treatment for preterm RDS. Available surfactant preparations include bovine- or porcine-derived products and synthetic surfactant preparations that are administered to preterm infants via endotracheal tube. Multiple studies have demonstrated the efficacy of exogenous surfactant in reducing newborn mortality and airleaks, especially when given as multiple doses early after birth in a prophylactic, as opposed to rescue, manner (22,23). Although a consistent reduction in the development of chronic lung disease (bronchopulmonary dysplasia) in preterm infants treated with surfactant has not been demonstrated, there is evidence that the severity of chronic lung disease has decreased in the era of surfactant therapy (24). Combined management strategies, for example, surfactant treatment and early extubation to continuous positive airway pressure (CPAP), show promise in decreasing not only the severity but the incidence of chronic lung disease in preterm infants with RDS as well (25,26).
Medicines in neonates
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Pulmonary surfactant is a complex mixture of phospholipids, neutral lipids and specific proteins. It lowers surface tension at the air-liquid interface of the lung to prevent alveolar collapse at end-expiration [1]. The major cause of neonatal respiratory distress syndrome (RDS) is a primary deficiency of surfactant [2], and surfactant replacement therapy has had a major impact in improving the outcome of this disorder in preterm infants [3]. Surfactants were the first drugs designed primarily for use in the newborn, and those licensed for treatment or prevention of RDS fall into 2 broad categories: synthetic and natural. Synthetic surfactants are composed mainly of phospholipids (usually dipalmitoylphosphatidylcholine, DPPC, also known as colfosceril palmitate) but do not contain surfactant proteins. Natural surfactants are derived from animal lungs, and they contain both phospholipids and surfactant proteins B and C [4].
Biochemical Adaptations to Early Extrauterine Life
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
José M. Medina, Carlos Vicario, María C. Juanes, Emilio Fernández
Pulmonary surfactant is composed of various Lipids and proteins that give rise to a phospholipid monolayer which lines lung lumen alveoli. This highly surface-active material decreases the surface tension at the air-liquid interface, reducing both the tendency of the alveoli to collapse at low transpulmonary pressures,24 and the transudation of fluid into the air spaces.25 A defect in the surfactant system causes respiratory distress syndrome in the newborn, which is due to a developmental deficiency of pulmonary surfactant in premature infants.26
Could Vitamin C Protect Against Mercuric Chloride Induced Lung Toxicity In The Offspring Rat: A Histological And Immunohistochemical Study
Published in Ultrastructural Pathology, 2021
Omnia I. Ismail, Manal M.S. El-Meligy
We have suggested that the damage in the type II pneumocytes led to produce insufficient pulmonary surfactant, which trigger a rise in the surface tension, therefore the collapse of alveoli was detected in our work. It was known that the pulmonary surfactant serves to reduce the surface tension of the alveolar lining and to keep the alveoli patent enabling efficient ventilation.26 We hypothesized that prenatal mercury exposure may promote the neonatal death owing to respiratory distress syndrome generating from deficient pulmonary surfactant. Additionally, other function of the type II pneumocyte acts as a progenitor for the type I pneumocyte, which is responsible for the gas exchange and lung maintenance. This mechanism plays a critical role in injury repair and regeneration. As during pulmonary injury, the type II pneumocyte proliferates and then differentiates into the type I pneumocyte that replaces the injured one and restores the structure of alveoli.27 Therefore, we proposed that the type II pneumocyte lost their proliferative and regenerative properities and the integration between both types of pneumocytes in the present work due to HgCl2 exposure.
Immunohistochemical analysis of protective effects of maternal fingolimod on the placenta and fetal lung and brain in chorioamnionitis-induced preterm birth rat model
Published in Immunopharmacology and Immunotoxicology, 2020
And Yavuz, Mekin Sezik, Serenat Eris Yalcin, Halil Asci, Ozlem Ozmen
Development of the central nervous system (CNS) is a very complex process. Interaction between neuron and glial cells is essential for mutual coherent development of various components of the nervous system. The glial cell, one of the chief cellular components of the nervous system, plays a pivotal role in the development of the CNS. Vimentin is necessary for nervous system development. Glial fibrillary acidic protein (GFAP) and vimentin are considered as major elements of astrocyte differentiation [20]. These intermediate filaments also play important roles in the pathological conditions of the CNS [21]. Apoptosis (programmed cell death) is evident in both physiological and pathological circumstances. Apoptosis is an essential feature of normal placental development, but is exacerbated in placental disease [22]. Cytokines are soluble, extracellular proteins that regulate immunologically regulated inflammatory reactions. A major function of the cytokines is their mediatory role in the interactions between the immune and the inflammatory systems. TNF-α and the interleukins are most important cytokines that indicate cellular damage in different tissues including the CNS [23,24]. The surfactant group is synthesized, assembled, transported, and secreted into the alveolus where it is degraded and then recycled. Metabolism of surfactants is slower in newborns, especially in preterm, than in adults. Defective pulmonary surfactant metabolism results in respiratory distress with attendant morbidity and mortality [25].
Inhalation of titanium dioxide (P25) nanoparticles to rats and changes in surfactant protein (SP-D) levels in bronchoalveolar lavage fluid and serum
Published in Nanotoxicology, 2019
Takami Okada, Byeong Woo Lee, Akira Ogami, Takako Oyabu, Toshihiko Myojo
Pulmonary surfactants are components of the lining fluid of lung alveoli and the first contact points of inhaled particles in the respiratory system. The surfactant secreted into the alveolar space is a lipoprotein complex produced in type II alveolar epithelial cells and Club cells. The major components of pulmonary surfactant are phospholipids and about 10% of the surfactant consists of proteins, four of which have been defined: SP-A, SP-B, SP-C and SP-D (Schleh et al. 2009; Wright 2005). Serum SP-D tests are conducted on patients with pulmonary diseases in hospitals. In our previous studies of rats administered crystalline silica, nickel oxide and multiwall carbon nanotubes by intratracheal instillation and inhalation, the pulmonary surfactants in BALF were effective biomarkers for assessing the hazardous property of these substances, allowing us to clarify the role of pulmonary surfactants in inflammation (Kuroda et al. 2006; Kadoya et al. 2012; Lee et al. 2013; Kadoya et al. 2016). Phospholipids, total protein, SP-D and BALF surface tension all correlated significantly with the polimorphonuclear neutrophils (PMNs) counts in BALF (Kadoya et al. 2016). If SP-D concentration in serum samples has any correlation with that in BALF samples, it will be feasible to analyze the SP-D level in serum samples of workers exposed to nanoparticles as a biomarker of the exposure.