PHYSIOLOGY OF RESPIRATION IN NEWBORN INFANTS AND IN THE RESPIRATORY DISTRESS SYNDROME

PEDIATRICS ◽  
1959 ◽  
Vol 24 (6) ◽  
pp. 1069-1101
Author(s):  
L. Stanley James

To improve our understanding of the respiratory distress syndrome, the importance of early examination of the infant, preferably at delivery, cannot be overemphasized. An attempt should be made to estimate clinically the degree of birth asphyxiation by a method such as the Apgar Score. The nature of respirations as well as the rate should be noted, particularly retractions and grunting. Decreased response to stimuli or poor tone, and a low blood pressure are significant signs. In this review, a number of comparisons have been drawn, including evidence from adult medicine or animal experiments. While these may appear unrelated, irrelevant or unduly speculative, they have been introduced for several purposes: to draw attention to aspects of the syndrome other than respiratory distress; to acquaint the general reader with more recent physiology which is deemed pertinent; and to emphasize the importance of relating one system to another, especially respiration to circulation. Many of the studies of respiratory function point to cardiac as well as pulmonary failure, notably the need for oxygen in the presence of a normal tidal and increased minute volume. Other circumstantial evidence of cardiac failure is abundant. Asphyxia appears to play a central role, affecting almost every system in the body and every phase of metabolism. It is probably responsible for the normal or low venous pressures occurring with a failing myocardium. It also accounts for the higher incidence of respiratory distress in the smaller prematures who are unable to achieve and maintain normal lung expansion. The syndrome is uncommon in larger full-term infants and in these instances is associated with obstetrical complications causing more severe degrees of birth asphyxia. The clinical picture includes a number of variations depending upon whether respiratory depression or symptoms relating to the central nervous or gastrointestinal systems predominate. Nevertheless, diagnosis of the respiratory distress syndrome should rely not on the presence or absence of membranes at necropsy, but rather on the history, symptoms and clinical signs. Inasmuch as asphyxia is not a disease, it would seem more logical to regard the syndrome as a failure in adaptation to extrauterine life. Failure to comprehend the many adaptations which newborn infants must make, both cardiopulmonary and biochemical, together with a narrow view centering only around the hyaline membranes, have for so many years cloaked this syndrome with mystery. Physiologic measurements in sick infants are difficult, and many of the determinations and calculations arduous. Some of the studies require confirmation, and others remain to be done, employing new or improved technics which are free from disadvantages of older methods. Because of many variables, caution should be exercised in drawing conclusions from a small number of cases. Early pioneering work has contributed greatly and has paved the way for future investigations. The value of serial studies correlated with careful clinical observations in order that the precise nature of a dynamic process may be more fully revealed has been clearly shown.

PEDIATRICS ◽  
1993 ◽  
Vol 92 (1) ◽  
pp. 135-139
Author(s):  
Hatem Khammash ◽  
Max Perlman ◽  
Julian Wojtulewicz ◽  
Michael Dunn

Objective. In light of the paucity of published data on the use of surfactant in full-term infants with respiratory failure due to meconium aspiration syndrome and respiratory distress syndrome, we report our experience with this therapy. Our goal was to explore possible justification for randomized controlled trials of surfactant treatment in similar patients at an earlier, less severe stage of the disease. Methods. Retrospective consecutive case series of 20 infants with severe meconium aspiration syndrome and 29 infants with severe respiratory distress syndrome who received bovine surfactant between March 1990 and December 1992 in three neonatal intensive care units in a regionalized setting. Outcome of treatment was assessed by comparing changes in several respiratory indices including the oxygenation index, between 4 and 6 hours and 1 and 3 hours before and after the first dose of surfactant. Differences were analyzed using analysis of variance for repeated measures, with treatment and time as co-variates. Results. In the meconium aspiration group the mean oxygenation index decreased from 36 ± 12 at 1 to 3 hours presurfactant to 24 ± 14 at 1 to 3 hours postsurfactant (P < .001). In the patients with respiratory distress syndrome the mean oxygenation index fell from 30 ± 17 at 1 to 3 hours presurfactant to 12 ± 6 at 1 to 3 hours postsurfactant (P = .0001). Three of 20 patients with meconium aspiration syndrome and 3 of 29 patients with respiratory distress syndrome received extracorporeal membrane oxygenation. Conclusions. Surfactant therapy in full-term infants with respiratory failure due to the meconium aspiration and respiratory distress syndromes is often effective in improving gas exchange. A randomized controlled trial of surfactant therapy at an earlier stage in the course of the illness should be performed.


2021 ◽  
pp. 30-41
Author(s):  
Tatyana Nikolaevna Tsyganova ◽  
Egor Egorov ◽  
Tamara Nikolaevna Voronina

COVID-19, a disease caused by the novel coronavirus SARS-CoV-2, primarily affects lung tissue and disrupts gas exchange, leading to acute respiratory distress syndrome, systemic hypoxia, and lung damage. The search for methods of prevention and rehabilitation, especially after suffering from pneumonia caused by COVID-19, is on the agenda. This article discusses the possibilities of the interval hypoxic training (IHT) method for preventing infections by initiating nitric oxide production in the body. One of the main effects of IHT is the balanced stimulation of nitric oxide (NO) secretion. Over the past two decades, there has been an increasing interest in the function of nitric oxide (NO) in the human body. Nitric oxide plays a key role in maintaining normal vascular function and regulating inflammatory processes, including those leading to lung damage and the development of acute respiratory distress syndrome (ARDS). Our immune system destroys bacteria and viruses by oxidative burst, i.e. when oxygen accumulates inside the cell. This process also involves nitric oxide, a signaling molecule that has an antibacterial and antiviral effect, as well as regulates vascular tone and affects the permeability of the cell wall. Interval hypoxytherapy enhances endogenous oxidative protection and increases the amount of nitric oxide, thus allowing the body’s cells to resist infection more effectively. Mitochondrial NOS induction and mitochondrial NO synthesis increase under the action of pathogenic factors on the cell. By modulating the activity of mtNOS and the synthesis of mitochondrial NO, it is possible to increase the resistance to hypoxic effects. Interval hypo-hyperoxic training as an effective non-specific method of increasing the body’s defenses is indispensable not only in the prevention of viral infection, but also in rehabilitation after viral pneumonia, as well as as a method that reduces the severity of viral infection in the event of infection.


1988 ◽  
Vol 112 (5) ◽  
pp. 778-781 ◽  
Author(s):  
Eduardo Dreizzen ◽  
Marek Migdal ◽  
Jean-Paul Praud ◽  
Jean-Francois Magny ◽  
Michel Dehan ◽  
...  

2020 ◽  
Author(s):  
Giorgia Testoni ◽  
Bárbara Olmeda ◽  
Jordi Duran ◽  
Elena López-Rodríguez ◽  
Mònica Aguilera ◽  
...  

Abstract The glycogenin knockout mouse is a model of Glycogen Storage Disease type XV. These animals show high perinatal mortality (90%) due to respiratory failure. The lungs of glycogenin-deficient embryos and P0 mice have a lower glycogen content than that of wild-type counterparts. Embryonic lungs were found to have decreased levels of mature surfactant proteins SP-B and SP-C, together with incomplete processing of precursors. Furthermore, non-surviving pups showed collapsed sacculi, which may be linked to a significantly reduced amount of surfactant proteins. A similar pattern was observed in glycogen synthase1-deficient mice, which are devoid of glycogen in the lungs and are also affected by high perinatal mortality due to atelectasis. These results indicate that glycogen availability is a key factor for the burst of surfactant production required to ensure correct lung expansion at the establishment of air breathing. Our findings confirm that glycogen deficiency in lungs can cause respiratory distress syndrome and suggest that mutations in glycogenin and glycogen synthase 1 genes may underlie cases of idiopathic neonatal death.


2015 ◽  
Vol 27 (1) ◽  
pp. 103
Author(s):  
Y. Liu ◽  
Y. Zhang ◽  
H.-S. Hao ◽  
W.-H. Du ◽  
H.-B. Zhu ◽  
...  

Developmental deficiency leads to low survival rates of newborns, especially in cloned animals. Alveoli collapse leading to respiratory failure is one of the major causes of death in newborn cloned calves. The present study provides an insight into the expression pattern of micro-RNAs (miRNAs) in lung tissues and their role in the respiratory distress syndrome (RDS) in the cloned calves. Short RNA high-throughput sequencing and bioinformatic analysis from small RNA libraries created from collapsed lung tissues from 4 newborn cloned calves with RDS and normal lung tissues from 4 age-matched healthy individuals were implemented. Lung tissues were collected by dissection from newborns that died due to RDS and from healthy individuals on the first day after birth. RNA samples from the lung tissues were processed to generate small RNA libraries that were further used for deep sequencing. Expression profiles of surfactant-associated protein B (SPB), surfactant-associate protein C (SPC), and their key transcription regulator thyroid transcription factor-1 (TTF-1), which are responsible for stabilising alveolar surface, reducing surface tension, and thus preventing alveoli collapse, were verified through real-time RT-PCR, Western blot, and immunohistochemistry (IHC). Differentially expressed (DE) miRNAs were quantified by edgeR (empirical analysis of digital gene expression data in R), and their target genes were predicted by both TargetScan and miRanda software. Only miRNAs with P values <0.05 were considered statistically significant (Fisher exact test). Sequence analysis revealed the presence of 1592 and 1777 miRNAs in the RDS and healthy groups, respectively. A total of 326 miRNAs were DE between the two groups according to our criteria, of which 179 miRNAs were up-regulated and 147 were down-regulated in the RDS group. Gene ontological analysis showed that the DE miRNAs had a primary role in DNA-dependent regulation of transcription, cytoplasm biosynthesis, and nucleotide binding. Eleven miRNAs (bta-miR-186, bta-miR-2284x_R+1, bta-miR-24–3p_R-2, bta-miR-424–3p, bta-miR-592_L-1, bta-miR-660, bta-miR-150_R-1, bta-miR-2478_L-2, bta-miR-450b_R-1, bta-miR-134_L+2R-2 and bta-miR-326_R+1) were DE between the 2 groups and were predicted to target SPB, SPC, and TTF-1, respectively. Among these DE miRNAs, 5 miRNAs (bta-miR-134_L+2R-2, bta-miR-424–3p, bta-miR-660, bta-miR-2478_L-2, bta-miR-450b_R-1) were up-regulated in the RDS group. Western blot and IHC confirmed the down-regulation of SPB, SPC, and TTF-1 at the protein level in RDS group. This increase in abundance of miRNAs targeting key regulatory genes in lung of newborn cloned calves may take part in the dysregulation of alveolus development leading to alveoli collapse and RDS. The assay for target gene verification and analysis of gene transcription profile are under study.Y. Liu and Y. Zhang contributed equally to this work. This project was supported by the National Natural Science Foundation of China (No. 31301977) and the National Nonprofit Institute Research Grant (No. 2011cj-11).


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