Neonatal Respiratory Diseases in the Newborn Infant: Novel Insights from Stable Isotope Tracer Studies

Carnielli, Virgilio P.; Giorgetti, Chiara; Simonato, Manuela; Vedovelli, Luca; Cogo, Paola

doi:10.1159/000444891

Cited by 8 publications

(10 citation statements)

References 81 publications

(111 reference statements)

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“…These are similar to the levels reported for rat (∼5 mg/kg) and rabbit (∼10 mg/kg) alveolar surfactant. Interestingly, these adult values are also similar to the alveolar surfactant levels of ∼5 (1–10) mg/kg in infants with RDS, implying that the high surfactant concentrations are specifically required at birth. ,,, …”

Section: What Do Physiological and Pathophysiological Studies Teach U...supporting

confidence: 59%

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Pulmonary Surfactant: A Mighty Thin Film

Possmayer,

Zuo,

Veldhuizen

et al. 2023

Chem. Rev.

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Pulmonary surfactant is a critical component of lung function in healthy individuals. It functions in part by lowering surface tension in the alveoli, thereby allowing for breathing with minimal effort. The prevailing thinking is that low surface tension is attained by a compression-driven squeeze-out of unsaturated phospholipids during exhalation, forming a film enriched in saturated phospholipids that achieves surface tensions close to zero. A thorough review of past and recent literature suggests that the compression-driven squeeze-out mechanism may be erroneous. Here, we posit that a surfactant film enriched in saturated lipids is formed shortly after birth by an adsorptiondriven sorting process and that its composition does not change during normal breathing. We provide biophysical evidence for the rapid formation of an enriched film at high surfactant concentrations, facilitated by adsorption structures containing hydrophobic surfactant proteins. We examine biophysical evidence for and against the compressiondriven squeeze-out mechanism and propose a new model for surfactant function. The proposed model is tested against existing physiological and pathophysiological evidence in neonatal and adult lungs, leading to ideas for biophysical research, that should be addressed to establish the physiological relevance of this new perspective on the function of the mighty thin film that surfactant provides.

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Section: What Do Physiological and Pathophysiological Studies Teach U...supporting

confidence: 59%

“…After birth, additional fluid uptake is facilitated by the lowered γ. − The lung inflation promoted by the presence of sufficient surfactant greatly facilitates this change. This reduction in lung fluid during the neonatal period can continue over a period of hours.…”

Section: What Do Physiological and Pathophysiological Studies Teach U...mentioning

confidence: 99%

Pulmonary Surfactant: A Mighty Thin Film

Possmayer,

Zuo,

Veldhuizen

et al. 2023

Chem. Rev.

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“…Surfactant is a complex mixture of lipids (90%) and four specific proteins (10%), surfactant proteins-A (SP-A), -B, -C and -D (10%). Of the surfactant lipids, 80-90% are phospholipids, the most abundant of which is the phosphatidylcholine (PC) class, the di-saturated dipalmitoylhosphatidylcholine (DPPC) and other phospholipids with saturated fatty acids in the one and two position of the glycerol moiety being the most critical for surfactant tension-active properties [67]. Glycerol is the main substrate for PC synthesis in the early neonatal period, when its concentration in circulation increases markedly, whereas later in life, glucose is the major source [68].…”

Section: Respiratory Distress Syndrome (Rds) and Surfactant Dysfunctionmentioning

confidence: 99%

Nutrients and Microbiota in Lung Diseases of Prematurity: The Placenta-Gut-Lung Triangle

et al. 2020

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Cardiorespiratory function is not only the foremost determinant of life after premature birth, but also a major factor of long-term outcomes. However, the path from placental disconnection to nutritional autonomy is enduring and challenging for the preterm infant and, at each step, will have profound influences on respiratory physiology and disease. Fluid and energy intake, specific nutrients such as amino-acids, lipids and vitamins, and their ways of administration —parenteral or enteral—have direct implications on lung tissue composition and cellular functions, thus affect lung development and homeostasis and contributing to acute and chronic respiratory disorders. In addition, metabolomic signatures have recently emerged as biomarkers of bronchopulmonary dysplasia and other neonatal diseases, suggesting a profound implication of specific metabolites such as amino-acids, acylcarnitine and fatty acids in lung injury and repair, inflammation and immune modulation. Recent advances have highlighted the profound influence of the microbiome on many short- and long-term outcomes in the preterm infant. Lung and intestinal microbiomes are deeply intricated, and nutrition plays a prominent role in their establishment and regulation. There is an emerging evidence that human milk prevents bronchopulmonary dysplasia in premature infants, potentially through microbiome composition and/or inflammation modulation. Restoring antibiotic therapy-mediated microbiome disruption is another potentially beneficial action of human milk, which can be in part emulated by pre- and probiotics and supplements. This review will explore the many facets of the gut-lung axis and its pathophysiology in acute and chronic respiratory disorders of the prematurely born infant, and explore established and innovative nutritional approaches for prevention and treatment.

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“…In 2016 he reported use of stable isotope tracer studies to evaluate neonatal respiratory diseases [31]. This year’s presentation was based on the assessment of lung growth in preterm infants by measuring oxygen diffusion during hospital stay.…”

mentioning

confidence: 99%