Pulmonary Surface Activity in Induced Pulmonary Edema*

Said, Sami I.; Avery, Mary Ellen; Davis, R. Kim; Banerjee, Chandra M.; El-Gohary, Mohammed A.

doi:10.1172/jci105159

Cited by 98 publications

(23 citation statements)

References 15 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although the nature of the forces responsible for this pericapillary pressure is not entirely clear, it seems that surface tension at the alveolar air-fluid interface may be involved (20). In particular, in the group II experiments of the present study, the heightened surface tension that occurs as fluid accumulates in alveoli (11,12) may, in turn, have contributed to the formation of edema.…”

Section: Introductionmentioning

confidence: 59%

See 1 more Smart Citation

The Application of Starling's Law of Capillary Exchange to the Lungs*

Levine¹,

Mellins²,

Senior³

et al. 1967

J. Clin. Invest.

124

View full text Add to dashboard Cite

Summary. The forces governing the movement of water across the pulmonary capillaries were studied in 39 intact, spontaneously breathing dogs. A situation favoring the net movement of water out of the pulmonary capillaries was created by means of partial pulmonary venous obstruction (left atrial balloon catheter) followed by rapid saline hemodilution. A predetermined difference between pulmonary capillary and plasma colloid osmotic pressures was maintained for periods of 1 to 2 hours. Left atrial (PLA) and plasma colloid osmotic pressures (7rp1) were measured directly. The water content of the lungs was measured serially by an indicator-dilution technique, and at autopsy by drying the lungs. The rate of accumulation of lung water was measured in four groups of animals: in three of the groups, the capillary hydrostatic and colloid osmotic pressures were varied; in the fourth group, the right lymphatic duct was obstructed in addition.The average rate of water accumulation in the lungs varied in a nonlinear way with the level of the capillary hydrostatic-plasma colloid osmotic pressure difference and was unaffected by the level of the capillary hydrostatic pressure. At low levels of PLA -7rpl, water accumulated in the lung at an average rate of 0.09 g per g dry lung per hour per mm Hg pressure difference.At higher levels of PLA -7rpl the average rate of accumulation was 0.22 g per g per hour per mm Hg AP; in most of the experiments in this group water accumulated in the lungs slowly during the first 30 minutes of the test period and more rapidly as the period was extended. Obstruction of right lymphatic duct outflow did not alter the rate of water accumulation. Based on the control data of the present experiments, the pericapillary pressure in normal lungs is estimated to be of the order of -9 mm Hg in the normal dog lung. The filtration coefficient for the pulmonary capillaries is estimated to be of the order of one-tenth to one-twentieth of that for canine muscle capillaries. The data of the present study indicate that edema formation in lung tissue cannot be defined solely in terms of intravascular forces, but may be governed to a significant degree by changes in pericapillary forces in the pulmonary interstitium.

show abstract

Section: Introductionmentioning

confidence: 59%

“…2) The force exerted by surface tension at the pulmonary air-fluid interface, which presumably affects pericapillary (and therefore transcapillary) pressure (10), would be expected to change progressively during pulmonary edema (11,12).…”

Section: Introductionmentioning

confidence: 99%

The Application of Starling's Law of Capillary Exchange to the Lungs*

Levine¹,

Mellins²,

Senior³

et al. 1967

J. Clin. Invest.

124

View full text Add to dashboard Cite

show abstract

“…Our results are in contrast to a hyperoxia study in the neonatal rat (24) which has reported no change in the air deflation PV curve in rats exposed to 80% oxygen for 6 d and decreased compliance in rats exposed to >95% oxygen; however, the lungs were degassed before measurement. The increased compliance in the air PV deflation curve of our 80% oxygen exposed neonatal mice may be due to a stiffening of lung tissue by collagen deposits or to edema, which could increase the tendency for alveolar collapse and lung recoil with lowering of distending pressure (25,26).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Dexamethasone on Chronic Pulmonary Oxygen Toxicity in Infant Mice

Ohtsu

et al. 1989

Pediatr Res

View full text Add to dashboard Cite

ABSTRACT. The effect of dexamethasone (0.1, 1, and 5 mg/kg/d given subcutaneously from d 14-18) was tested in infant mice continuously exposed from birth to either humidified air or 80% oxygen. Dexamethasone significantly decreased lung wet wt ( p < 0.01), lung water ( p < 0.021), lung dry wt, protein, and DNA ( p < 0.001) in both airand oxygen-exposed animals. Dexamethasone, however, had no effect on lung compliance measured after animals were killed on d 18. It also had no effect on the increase in the blood-air barrier thickness or decrease in the blood-air exchange surface area seen in the 80% oxygen-exposed mice. Dexamethasone decreased thymus gland wt ( p < 0.001), body wt gain ( p < 0.001), brain wt ( p < 0.001), and lung lymphocytes ( p < 0.05) in both air-and oxygen-

show abstract

“…of the alveolar epithelium, and contamination of the alveolar spaces with protein-rich material that inhibits the surface activity. It was suggested more than a decade ago that surfactant inhibition occurs (28), and recent evidence indicates that surfactant is inhibited in immature lambs (15) treated with exogeneous surfactant, oxygen and artificial ventilation. Our data demonstrate that similar inhibition can occur in mature rat lungs, despite apparently normal surfactant phospholipids.…”

Section: Discussionmentioning

confidence: 99%

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

et al. 1984

View full text Add to dashboard Cite

Summaryoxygen exposure with simultaneous intravenous hypoxanthine infusion. Lung injury was induced in young rats by a continuous infusion of hypoxanthine intravenously and breathing 100% oxygen for 48 h (group 1). Control animals were rats infused glucose and MATERIALS AND METHODSbreathing 100% oxygen (group 2), rats infused hypoxanthine in room air (group 3), and untreated rats (group 4). In group 1 rats interstitial and alveolar edema was found with a tendency toward marked margination of polymorphonuclear neutrophils in small vessels (P < 0.025 compared with group 2). The main elastase inhibitor alphal-antitrypsin (a-1-PI) was significantly elevated in group 1; 2-, 3-and 5-fold, respectively, when compared with groups 2, 3, and 4. The surfactant phopholipids from alveolar lavage were normal in all groups. The protein-rich fraction of the lavage fluid from group I rats inactivated, however, the surface properties of lung surfactant. Minimum surface tension in group 1 rats was 14.5 dyn/cm compared with 7.0 dyn/cm in group 2, 2.9 dyn/cm in group 3 and 3.5 dyn/cm in group 4 (P < 0.05, group 1 and 2 versus 4). We conclude that the combination of hypoxanthine and high levels of oxygen causes lung injury, possibly via free oxygen radicals. We discuss the possibility that these findings demonstrate a basic pathogenetic mechanism for the hypoxic-hyperoxic insult and can contribute to the understanding of pathogenesis of a variety of diseases both in pediatrics and adult medicine. AbbreviationFree oxygen radicals have been shown to destroy cell membranes by lipid peroxidation (3, 8, 1 1, 2 1). It has been suggested that such radicals play an important role in the pathogenesis of the acute and chronic lung damage among patients treated with oxygen. Many authors have, however, suggested that oxygen must be combined with other more or less unknown factors, before injury occurs ( 14,27).Recently, it has been shown that the hypoxanthine/xanthine oxidase system generates free radicals (7), and that this system potently induces inflammatory changes both in the hamster cheek pouch (22) and the rat lung (16). Further, it has, by now, been well established that hypoxanthine accumulates in tissues (33), plasma (30,32,34,35), and other body fluids (12,23,25) during hypoxia. When high concentrations of oxygen are administered to the hypoxic patient, large amounts of free radicals may be produced by the hypoxanthine/xanthine oxidase system. We, therefore, have raised the question whether the combination of hypoxanthine and oxygen is more damaging than high oxygen alone to the lung. In the present study we evaluated this by investigating experimentally the effect on the rat lung to 100% Young female rats of the Wistar strain, weighing 170-230 g, were used. Four groups were investigated. Group 1, rats infused continuously with 5 mM hypoxanthine dissolved in 5% glucose and exposed to 98-100% oxygen (n = 10). Group 2, rats infused continuously with 5% glucose and exposed to 98-100% oxygen (n = 9). Group 3, rats infused continuously wit...

show abstract

Pulmonary Surface Activity in Induced Pulmonary Edema*

Cited by 98 publications

References 15 publications

The Application of Starling's Law of Capillary Exchange to the Lungs*

The Application of Starling's Law of Capillary Exchange to the Lungs*

The Effect of Dexamethasone on Chronic Pulmonary Oxygen Toxicity in Infant Mice

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

Contact Info

Product

Resources

About