Lung Surfactant: Cellular and Molecular Processing

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The adequacy of pulmonary surfactant is maintained by unique and highly regulated systems mediating the synthesis, secretion, reutilization, and catabolism of surfactant. Loss or inactivation of pulmonary surfactant later in life occurs in the adult respiratory distress syndrome ARDS , a significant cause of morbidity and mortality following infection, shock, or trauma.

The Respiratory System: Pulmonary Surfactant

This chapter reviews the biology of the surfactant system and its implications for the pathogenesis, diagnosis, and treatment of respiratory disease in premature infants and adults. Suggested reviews of these topics are provided in the References section.

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Avery and Mead associated the lack of a lipid-rich material in the lungs of infants dying from idiopathic respiratory distress syndrome with alveolar collapse and respiratory failure. A surface film composed of multilayered sheets of phospholipids creates a distinct phase separating air and liquid, reducing surface tension to nearly zero and maintaining residual lung volume at end expiration.

Complex interactions between surfactant phospholipids and proteins are required to maintain surfactant film throughout life. Pulmonary surfactant lipids and proteins are synthesized and secreted by alveolar type II epithelial cells into the alveoli, where they form multilayered lipid-rich films that reduce surface tension to maintain ventilation Figs.

Pulmonary alveolar ultrastructure.

Surfactant phospholipid metabolism

The air—blood barrier is comprised of the capillary endothelium above the dotted orange line and the closely apposed type I epithelial cell below the dotted orange line. The dotted blue line delineates the interstitial space between endothelial cells and type II epithelial cells with their specialized secretory lipid organelles lamellar Forgot Password?

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About MyAccess If your institution subscribes to this resource, and you don't have a MyAccess Profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus. Sign in via OpenAthens. The surfactant monolayer is in charge of reducing the surface tension upon compression i. These conflicting requirements are achieved by a combination of specialised compounds that work synergistically to promote adsorption and spreading during dynamic compression—expansion cycling. DPPC alone can generate near-zero surface tension at the air—water interface during compression, but cannot respread fast enough upon expansion because it forms highly cohesive semi-crystallised liquid-condensed two-dimensional domains at the air—water interface due to strong lateral interactions.

It is the presence of unsaturated lipids such as phosphatidylglycerols and phosphatidylcholines, and of the amphiphilic proteins SP-B and SP-C that allows reversion to the fluid liquid-expanded phase. Therefore, in order to reach low tensions some minor components pre-dominantly non-phosphatidylcholine compounds are squeezed out from the monolayer upon compression, which results in an enrichment of the monolayer in DPPC and allows transition to the condensed phase.

Surface tension is then reduced while alveolar collapse is prevented.

Surfactant Deficiency | SpringerLink

By contrast, in ARDS and ALI, inactivation is rapid and often correlated with increased concentration of various substances, including plasma proteins, unsaturated phospholipids, lysophospholipids, free unsaturated acids e. Various in vitro studies have reported that different inhibitors, including plasma proteins and certain lipids, can interfere at different stages with phospholipid functions by hindering phospholipid adsorption and formation of a functional surfactant film, by preventing the film from reaching low interfacial tensions or by increasing film compressibility, and by affecting phospholipid re-spreading from surfactant reservoirs upon expansion.

This view has recently been confirmed by a study of the rheological dilational properties of surface films formed by Exosurf, Survanta, Curosurf or Alveofact in the presence of albumin and PVP, PEG or dextran. The hydrophilic polymers were found to restore the DPPC content of the surface film. In another recent study, the effect of hydrophilic polymers was investigated using thin black foam films. The ability of the polymers to decrease the effect of albumin inhibition was expressed by their capacity of restoring stable and homogeneous black films Fig.

A microinterferometric method allowed direct visualisation of foam film morphology, evaluation of its stability and viscosity, and provided access to the disjoining pressure, a measure of the interactions electrostatic, van der Waals, steric, etc. This study indicated that some specific interactions might take place, as certain polymers have an effect on certain surfactant substitutes, but not on all of them e.

It would obviously be impracticable to use high levels of saline because of their osmotic effect on lung tissue. PLV with FC has been described in many animal models premature, full-term neonatal and adults and a few human studies. Improved oxygenation and lung compliance were achieved in preterm animal models, 90 as well as in premature infants. A study on a saline lavage rabbit model of respiratory failure showed improvement in oxygenation with PFOB, effective gas exchange at relatively low airway pressures, and overall improvement in both pulmonary mechanics and lung histology as compared with conventional ventilation.

A human adult trial found significant improvement in physiological shunt and static pulmonary compliance. The sequence of pro-inflammatory and anti-inflammatory cytokines exhibited an anti-inflammatory effect in the alveolar environment with reduction of pro-inflammatory interleukins IL-1 and IL-6, white blood cell count, and protein capillary leak.

Administration of PFOB reduced total white cell and neutrophil infiltration into the alveoli, capillary leak of proteins, and expression of the inflammatory cytokines IL-b and IL The anti-inflammatory IL was also reduced. All of these alveolar responses appeared to be beneficial when viewed individually, but did not result in significant clinical improvement. The fact that FCs attenuate the pro-inflammatory and pro-coagulatory responses of activated monocytes and of alveolar macrophages may contribute to the protective role of FCs in injuries associated with local activation of inflammatory processes.

The images were obtained using the fluorescent dye NBDC6-HPC, which is preferentially soluble in the disordered regions of the monolayer. Recently, an equation of state for insoluble monolayers was applied to describe the isotherms of phospholipids measured in the presence of a fluorocarbon in the gas phase. Due to the interaction of the adsorbed FC molecules with DPPC, the mutual interaction energy between DPPC molecules is reduced, leading to a very effective fluidization of the monolayer.


First, prolonged oscillations were applied to a DPPC monolayer adsorbed on the surface of an air bubble Fig. Similar values have been measured for DPPC at equilibrium using different techniques. Chronic obstructive pulmonary disease COPD is a lung disease characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible.

The pathophysiological mechanisms of acute renal dysfunction during acute decompensation of pulmonary hypertension are similar to those observed in type I cardiorenal syndrome. Patients with acute respiratory distress syndrome ARDS often have lung surfactant that lacks the full range of surface tension modulation upon compression [2]. In contrast to acute pulmonary embolism, chronic thromboemboli are often complete occlusions or non-occlusive filling defects in the periphery of the affected vessel which form obtuse angles with the vessel. Acute Ischemic Stroke Class II Recommendation Class, Level of Evidence LOE Usefulness of chest radiographs in the hyperacute stroke setting in the absence of evidence of acute pulmonary, cardiac or pulmonary vascular disease is unclear.

Acute bovine pulmonary edema and emphysema ABPE is a nat-urally occurring illness in cattle. Idiopathic Pulmonary Fibrosis Prognosis: An Overview Idiopathic pulmonary fibrosis IPF is a progressive disease, meaning that it does not improve on its own or with treatment. Pulmonary embolism and deep venous throm-bosis are two manifestations of one pathologic process.

Knowing that someone in the family had or has pulmonary hypertension should prompt you to seek early evaluation should symptoms occur. The most accurate way to determine if a lung disease affects this part of the lung is with a surgical biopsy. Hematogenous dissemination frequently occurs, especially in an immunocompromised host. As the disease begins to spread through the lungs, it leads to end stage pulmonary fibrosis. Therefore, the purpose of this systematic re-view and meta-analysis is to summarize available evidence on the predictive value of commonly used CT severity parameters for short-term clinical outcomes in acute pulmonary embolism.

Acute Lung Injury Research. A pulmonary embolism PE can cause symptoms such as chest pain or breathlessness but may have no symptoms and be hard to detect. Acute PE increases pulmonary vascular resistance, partly attributable to hypoxic vasoconstriction.

This finding prompted a revision in the consensus definition of a favorable response to acute vasodilator testing. Redistribution of extravascular fluid from the periphery into dependent areas when supine i. It is uncertain if and how individuals with COPD differ from former smokers without airflow obstruction in their response to naturally occurring episodes of particulate air pollution. Only when clinical data and radiographic findings are correlated can patient care be optimized.

At pulmonary rehabilitation you'll work with a team of specialists who will help you improve your physical condition so you will stay healthy and active. Pulmonary fibrosis is a lung disease that occurs when lung tissue becomes damaged and scarred. While prednisone is not usually used to treat idiopathic pulmonary fibrosis, it is sometimes used to treat inflammation in the lungs of people living with other forms of pulmonary fibrosis. Discuss the components of a focused pulmonary assessment.

With PPHN the baby does not change over from fetal to normal newborn circulation. The tests measure lung volume, capacity, rates of flow, and gas exchange. Sweidan, Navneet K. Sometimes, an acute illness, such as the common cold, will just go away on its own. Pulmonary exacerbations are common among people with cystic fibrosis, yet little is known about best treatment practices. Acute respiratory distress syndrome is the clinical manifestation of severe, acute lung injury. Acute respiratory failure occurs when fluid builds up in the air sacs in your lungs.

Chronic obstructive pulmonary disease COPD is a common problem in the elderly. ARDS is an example of acute inflammation not only persisting but also becoming amplified to involve the entire organ. The regulation at 42 CFR However the x-ray is.


Advances in imaging have enabled more detailed patient assessment, but pulmonary hypertension continues to be a life shortening condition, and there is often a delay of around two years from onset of symptoms to diagnosis. That can make it hard for you to breathe. The congestion of the left nasal turbinates means that at the time of the MRI, you had congestion in that area.

Causes of AKI include those that damage the kidneys, leading to the inability of the kidneys to perform their function. Without proper treatment and support. We participate in the NRMP subspecialty match. If leads V1 and V2 are inverted in conjunction with an S1Q3T3 pattern, this is a very specific finding in acute pulmonary embolism or other acute cor pulmonale process. Williams, Steven H. A critical appraisal of the morphine in the acute pulmonary edema: real or real uncertain? Acute heart failure AHF is the leading cause of hospitalization and consultation in hospital emergency department ED in industrialized nations 1,2 , and its prevalence increases with age 1.

I have quit smoking and have a breathing test on the First: Keep an eye on it. In terms of pathologic diagnosis, an embolus is acute if it is situated centrally within the vascular lumen or if it occludes a vessel vessel cutoff sign see the first image below. Pulmonary hypertension may also be caused by other conditions, and in some cases, the cause is unknown. Track Manuscript. In some people, the lung tissue quickly becomes thick and stiff, while in others, the process is much slower.

Advanced Process. The differential diagnosis of pulmonary opacities in patients with hematologic ma-lignancies is broad and includes both infectious and noninfectious causes. Pulmonary tuberculosis TB is a contagious, infectious disease that attacks your lungs. You may also use this system to track your manuscript through the review process.

Pulmonary congestion and edema develops in two stages. Pulmonary edema is always secondary to an underlying disease process and thus the ability to distinguish the cause of excess interstitial lung fluid is critical for its treatment. Symptoms include coughing, shortness of breath, and trouble exercising. Noncardiogenic causes of pulmonary edema include things like pulmonary infections, inhalation of toxic substances, and trauma to the chest.

Acute pulmonary oedema has a high mortality. The signs and symptoms of acute respiratory failure reflect the underlying disease process and the associated hypoxemia or hypercapnia. It requires emergency management and usually admission to hospital. Normally blood flows from the right side of the heart into the pulmonary arteries and smaller blood vessels in the lungs. Here are the facts you need to know about end stage pulmonary fibrosis. Witt, John R. Histoplasmosis can spread to other organs through the bloodstream dissemination. Perfusion lung scanning was used to assess the change in pulmonary perfusion at 24 hours and seven Treatment of thrombosis by activation of the plasma.

Stage 2: Combination of alveolar overflow and interstitial consolidations.

Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing Lung Surfactant: Cellular and Molecular Processing
Lung Surfactant: Cellular and Molecular Processing

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