Altered surface tension of lung extracts and lung mechanics

Tierney, Donald F.; Johnson, Rudolph P.

doi:10.1152/jappl.1965.20.6.1253

Cited by 130 publications

(54 citation statements)

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“…(18) Lung injury induced by mechanical ventilation is multifactorial and includes the structural disruption generated by lung overdistension and by the shear forces created during repetitive opening and closing of atelectatic regions. Mechanical ventilation has also deleterious effects on the surfactant function, increasing the tendency of distal airways and alveoli to collapse, and increasing the pressure necessary to open the lung (20,21). Although the higher airway pressures achieved may result in increased transmural capillary pressure, facilitating the development of hydrostatic edema, the lung injury induced by high V T includes alterations in the pulmonary capillary permeability and alveolar epithelium leaks (22).…”

Section: Discussionmentioning

confidence: 99%

Ventilation with high tidal volume induces inflammatory lung injury

Bueno

Santos

et al. 2002

Braz J Med Biol Res

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Mechanical ventilation with high tidal volumes (V T ) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH 2 O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO 2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-α concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-α concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-α in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Ventilation with high tidal volume induces inflammatory lung injury

Bueno

Santos

et al. 2002

Braz J Med Biol Res

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“…Thus, a decrease in surfactant synthesis could account for the mechanical and histological changes seen in oxygen toxicity. This situation could be further aggravated by capillary destruction (24) and leakage into the alveolar spaces of blood components which inactivate surfactant (28). …”

Section: Discussionmentioning

confidence: 99%

Hyperoxia: Influence on Lung Mechanics and Protein Synthesis

Gacad¹,

Massaro²

1973

J. Clin. Invest.

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A B S T R A C T We studied the time-course of the influence of in vivo hyperoxia on lung mechanics and on protein synthesis. After 24 h of exposure to greater than 98% 02 at 1 atm there were no alterations in descending pressure-volume curves (air or saline) of lungs excised from O2-exposed rats compared to control rats. After 48 h of hyperoxia there was a decrease in lung compliance.To study protein synthesis, as indicated by L-[U-'4C] leucine incorporation into protein, lung slices were incubated with L-[U-J4C] leucine and surface-active material then obtained by ultracentrifugation of lung homogenates. We measured radioactivity in total protein and in protein in the surface-active fraction. There were no alterations in incorporation after 12 h of hyperoxia. After 24 h of hyperoxia there were significant decreases (P < 0.05) in L-[U-24C]leucine incorporation into total protein and into protein of the surface-active fraction. After 48 h of hyperoxia incorporation into protein of the surface-active fraction was decreased to a greater extent than incorporation into total protein, 63±4% and 75+5%, respectively, (P < 0.025).These studies show that hyperoxia produces a major decrease in protein synthesis, including synthesis of protein in a surface-active fraction, before the onset of any detectable changes in the static compliance of excised lungs.

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“…This irreversibility coincides with the development of atelectasis, hemorrhage, and edema in the occluded lung, which in turn has been attributed to loss ofthe alveolar surface lining material, surfactant (8)(9)(10). Although the ability of pulmonary surfactant to reduce surface tension is decreased after pulmonary artery occlusion, it remains unclear whether this alteration in function contributes to the development or results as a consequence of the alveolar edema and hemorrhage that occur (8,(11)(12)(13). If pulmonary surfactant is actually quantitatively depleted after pulmonary artery occlusion, as suggested by Morgan and Edmunds (14), then type II alveolar pneumocytes might show depletion of their lamellar bodies (LB)', which are recognized as the intracellular storage sites of the surface active phospholipids.…”

Section: Introductionmentioning

confidence: 99%

Lamellar body depletion in dogs undergoing pulmonary artery occlusion.

Shepard¹,

Hauer²,

Miyai³

et al. 1980

J. Clin. Invest.

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A B S T R A C T We have investigated the relationship between pulmonary artery occlusion (PAO) and the surfactant system of the lung by studying the ultrastructural responses of type II alveolar pneumocytes to PAO of 4-12 h duration in 16 mongrel dogs. In six of these animals, the occluded lung was allowed to reperfuse for 6 h before killing and in four animals subjected to PAO of 4 h duration, the occluded lung was ventilated with 5% CO2 balance air. PAO by itself resulted in a dramatic 80% reduction in the volumetric density of lamellar bodies (LB) in the type II cells. This resulted predominantly from a decrease in volume of the individual LB. Although reperfusion was associated with an increase in LB volume density toward normal, 6 h of reperfusion was insufficient to re-establish normal type II cellular morphology. Ventilation of the occluded lung with 5% CO2 prevented LB depletion indicating that alveolar CO2 tension may affect the release and/or synthesis of LB in type II pneumocytes.

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Altered surface tension of lung extracts and lung mechanics

Cited by 130 publications

References 0 publications

Ventilation with high tidal volume induces inflammatory lung injury

Ventilation with high tidal volume induces inflammatory lung injury

Hyperoxia: Influence on Lung Mechanics and Protein Synthesis

Lamellar body depletion in dogs undergoing pulmonary artery occlusion.

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