Surfactant homeostasis in the rat lung during swimming exercise

Nicholas, Terence E.; Power, John H.; Barr, Heather A.

doi:10.1152/jappl.1982.53.6.1521

Cited by 62 publications

(36 citation statements)

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“…For (1), and, in adult rats, exercise (swimming) was associated with an increase in alveolar surfactant pools (2). Furthermore, 15 min of ventilation with high tidal volume caused release and/or secretion of surfactant (3), and in isolated perfused lungs given a single high tidal volume breath, surfactant pools were increased in rat lung lavage (31).…”

Section: Discussionmentioning

confidence: 99%

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Mechanical Ventilation Effect on Surfactant Content, Function, and Lung Compliance in the Newborn Rat

et al. 2004

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Studies of ventilator-associated lung injury in adult experimental animal models have documented that high tidal volume (TV) results in lung injury characterized by impaired compliance and dysfunctional surfactant. Yet, there is evidence that, in neonates, ventilation with a higher than physiologic TV leads to improved lung compliance. The purpose of our study was to evaluate how lung compliance and surfactant was altered by high TV ventilation in the neonate. We utilized a new model (mechanically air-ventilated newborn rats, 4 -8 d old), and used 40 or 10 mL/kg TV strategies. Age-matched nonventilated animals served as controls. In all animals, dynamic compliance progressively increased after initiation of mechanical ventilation and was significantly greater than basal values after 60 min (p Ͻ 0.01). Lung lavage total surfactant with both TV strategies (p Ͻ 0.05) and the large aggregate fraction (only in TV ϭ 40 mL/kg; p Ͻ 0.01) were significantly increased by 60 min of mechanical ventilation, compared with control animals. Ventilation with 40 mL/kg TV for 60 min adversely affected the lung surfactant surface-tension lowering properties (p Ͻ 0.01). After 180 min of ventilation with 40 mL/kg TV, the lung total surfactant content and dynamic compliance values were no longer distinct from the nonventilated animals' values. We conclude that, in the newborn rat, mechanical ventilation with a higher than physiologic TV increases alveolar surfactant content and, over time, alters its biophysical properties, thus promoting an initial but transient improvement in lung compliance. A single stretch of alveolar type II cells causes an increase in cytosolic calcium resulting in stimulation of surfactant secretion for up to 30 min post stretch (1). In adult animals, this mechanism is operative after an increase in spontaneous breathing tidal volume (2, 3), but never demonstrated after short-term mechanical ventilation with a higher than physiologic tidal volume.Isolated adult rat lungs mechanically ventilated with a tidal volume four times higher than physiologic (25 mL/kg) for 1 h showed a decrease in lung compliance (4), which was associated with an increased conversion from LA to SA within the alveolar space (5). These latter changes likely accounted for the reduction in compliance, inasmuch as adequate biophysical activity of surfactant is dependent on a functional LA fraction.The concept that high tidal volumes may have adverse effects has been consistently demonstrated in multiple animal models of adult ventilator-associated lung injury (6 -8). This concept has driven a variety of strategies aimed at reducing tidal stretch, including permissive hypercapnia (9 -11), as well as studies designed to limit pressure and volume ventilatory parameters associated with tidal stretch (12-14). Indeed, in

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Section: Discussionmentioning

confidence: 99%

“…(1). In adult animals, this mechanism is operative after an increase in spontaneous breathing tidal volume (2,3), but never demonstrated after short-term mechanical ventilation with a higher than physiologic tidal volume.…”

mentioning

confidence: 99%

Mechanical Ventilation Effect on Surfactant Content, Function, and Lung Compliance in the Newborn Rat

et al. 2004

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“…Maximum stimulation by agonists in the absence of stretch forces can induce a secretory rate of about 8% per hour in vitro [87]. Hyperventilation, however, was shown to increase the secretory rate 14 fold [88]. Since the effects of agonists are modest, the majority of surfactant secretion seems to be stimulated by ventilation-induced physical forces.…”

Section: Regulatory Aspects Of Surfactant Synthesis and Secretionmentioning

confidence: 99%

The role of pulmonary surfactant in obstructive airways disease

Hohlfeld

Fabel²,

Hamm³

1997

Eur Respir J

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Pulmonary surfactant research has an increasing impact on treatment considerations in adult respiratory disorders, above all acute respiratory distress syndrome (ARDS). Obstructive airways diseases have only been sporadically addressed in this respect. In the last decade, direct and circumstantial evidence for surfactant as a contributing factor in the regulation of airway calibre has emerged.Morphologically, a bronchiolar surfactant layer has been demonstrated, whereby the airways are mostly supplied by alveolar surfactant components via the mucociliary escalator. Functionally, prevention of airway film collapse and collapse of the airway walls are important surfactant properties in maintaining airway stability. In addition to its surface activity, airway surfactant improves bronchial clearance and regulates airway liquid balance, thus indirectly modulating airway wall thickness and airway diameter. Surfactant has furthermore been shown to modulate the function of respiratory inflammatory cells. Its immunomodulatory activity includes suppression of cytokine secretion and transcription factor activation. This may be of importance in the inflammatory network of asthma.Thus, dysfunction of surfactant in obstructive lung disease might be one of the mechanisms leading to increased airway resistance, which is commonly thought to be due to narrowing of airways under humoral and nervous control. In animal models of asthma, surfactant dysfunction was demonstrated, which was possibly due to protein inhibition. Furthermore, surfactant therapy seems to be capable of preventing allergen-induced bronchoconstriction. Human studies on surfactant impairment in obstructive airways diseases are still scarce but the data available are consistent with animal studies.Antiobstructive pharmacotherapy, mainly with corticosteroids, might influence and improve airway surfactant balance, but the exact mechanisms and the overall effect of pharmacotherapy on surfactant function in obstructive airways disease has to be further elucidated. Our knowledge about the role of pulmonary surfactant in obstructive airways disease is still limited, but there is convincing evidence that pulmonary surfactant plays a role in keeping the airways open.

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“…In rats, swimming also results in a stimulation of surfactant secretion within minutes (37). A direct mechanical stimulus is partially responsible for the increase in surfactant, as in vitro, physical stretch of isolated type II cells results in an increase in surfactant secretion equivalent to a combination of agonists (16,66).…”

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confidence: 97%

Control of the development of the pulmonary surfactant system in the saltwater crocodile,Crocodylus porosus

Sullivan

Orgeig

Daniels

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. Control of the development of the pulmonary surfactant system in the saltwater crocodile, Crocodylus porosus. Am J Physiol Regul Integr Comp Physiol 283: R1164-R1176, 2002. First published July 25, 2002 10.1152/ ajpregu.00009.2002.-Pulmonary surfactant is a mixture of lipids and proteins that controls the surface tension of the fluid lining the inner lung. Its composition is conserved among the vertebrates. Here we hypothesize that the in ovo administration of glucocorticoids and thyroid hormones during late incubation will accelerate surfactant development in the saltwater crocodile, Crocodylus porosus. We also hypothesize that the increased maturation of the type II cells in response to hormone pretreatment will result in enhanced responsiveness of the cells to surfactant secretagogues. We sampled embryos at days 60, 68, and 75 of incubation and after hatching. We administered dexamethasone (Dex), 3,5,3Ј-triiodothyronine (T3), or a combination of both hormones (Dex ϩ T3), 48 and 24 h before each prehatching time point. Lavage analysis indicated that the maturation of the phospholipids (PL) in the lungs of embryonic crocodiles occurs rapidly. Only T3 and Dex ϩ T3 increased total PL in lavage at embryonic day 60, but Dex, T3, and Dex ϩ T3 increased PL at day 75. The saturation of the PLs was increased by T3 and Dex ϩ T3 at day 68. Swimming exercise did not increase the amount or alter the saturation of the surfactant PLs. Pretreatment of embryos with Dex, T3, or Dex ϩ T3 changed the secretion profiles of the isolated type II cells. Dex ϩ T3 increased the response of the cells to agonists at days 60 and 68. Therefore, glucocorticoids and thyroid hormones regulate surfactant maturation in the crocodile.

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Surfactant homeostasis in the rat lung during swimming exercise

Cited by 62 publications

References 0 publications

Mechanical Ventilation Effect on Surfactant Content, Function, and Lung Compliance in the Newborn Rat

Mechanical Ventilation Effect on Surfactant Content, Function, and Lung Compliance in the Newborn Rat

The role of pulmonary surfactant in obstructive airways disease

Control of the development of the pulmonary surfactant system in the saltwater crocodile,Crocodylus porosus

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