Interstitial Pulmonary Edema Research Articles

Interstitial Pulmonary Edema in Acute Malaria

Reversible interstitial pulmonary edema occurred as a complication of acute malaria in the absence of detectable cardiac decompensation, renal impairment, cerebral dysfunction, or fluid retention. This pattern is attributed to transient alteration in pulmonary capillary permeability and may be the result of hypersensitivity.

Regional lung function in patients with hepatic cirrhosis.

The lung volume at which the dependent lung zones begin to trap gas as a result of airway closure (i.e., the "closing volume") was measured with (133)Xe in 10 seated patients with hepatic cirrhosis. In all of them the closing volume was increased above normal, and in eight it was greater than the functional residual capacity, indicating the presence of airway closure and gas trapping during resting tidal volume breathing. Direct measurements made with (133)Xe in five cirrhotic patients (a) confirmed the presence of increased gas trapping in the lower lung zones both at residual volume and at functional residual capacity, and (b) indicated that in liver cirrhosis the ventilation-perfusion ratio of the dependent lung zones may be very low, primarily as a result of decreased ventilation due to airway closure. It is concluded that in hepatic cirrhosis, gas trapping in the dependent lung zones may be an important cause of impaired gas exchange within the lungs. It is suggested that the premature airway closure observed in this disease may be due to mechanical compression of small airways by dilated blood vessels and/or interstitial pulmonary edema.

Histamine and interstitial pulmonary edema in the dog.

Histamine, administered to dogs by various routes, produced peribronchial interstitial edema. Using colloidal carbon as an electron-dense tracer, it was shown that bronchial venules had become leaky at the same time that the minute blood vessels of the pulmonary circulation remained unaffected by the histamine. The effect of histamine was rapid and brief in duration: wide interendothelial gaps appeared in the walls of bronchial venules through which blood and tracer escaped into the interstitium. This action of histamine seemed to be related to the presence in the bronchial venular endothelium of abundant cytoplasmic fibrils that presumably have contractile capacity. Water content of the lungs was consistent with morphologic evidence that histamine promoted the accumulation of fluid in the lungs. The same pattern of response was observed after bradykinin or compound 48/80, a mast cell degranulator. In contrast to these three agents, serotonin did not affect bronchial venular permeability to colloidal carbon. Consideration of these observations in the light of the large extent of the bronchial venular plexus, raises the possibility that the bronchial venular system may play an important reabsorptive role under normal circumstances and that it may also be involved in the genesis of certain types of interstitial pulmonary edema.

Effects of posture and exercise on the pulmonary extravascular water volume in man.

ArticleEffects of posture and exercise on the pulmonary extravascular water volume in man.B E Marshall, R L Teichner, T Kallos, H J Sugerman, M Q Wyche Jr, and K R TantumB E Marshall, R L Teichner, T Kallos, H J Sugerman, M Q Wyche Jr, and K R TantumPublished Online:01 Sep 1971https://doi.org/10.1152/jappl.1971.31.3.375MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByExercise-induced interstitial pulmonary edema at sea-level in young and old healthy humansRespiratory Physiology & Neurobiology, Vol. 191Studies on the cell biology of interendothelial cell gapsCristhiaan D. Ochoa, and Troy Stevens1 February 2012 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 302, No. 3Impairment of 3000-m Run Time at Altitude Is Influenced by Arterial Oxyhemoglobin SaturationMedicine & Science in Sports & Exercise, Vol. 43, No. 9Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edemaAlastair N. H. Hodges, A. William Sheel, John R. Mayo, and Donald C. McKenzie1 July 2007 | Journal of Applied Physiology, Vol. 103, No. 1Evidence of pulmonary oedema triggered by exercise in healthy humans and detected with various imaging techniquesActa Physiologica, Vol. 189, No. 4Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists12 January 2007 | European Journal of Applied Physiology, Vol. 99, No. 6Extravascular Lung Water and Peripheral Volume Status in Hemodialysis Patients With and Without a History of Heart FailureASAIO Journal, Vol. 52, No. 4Determining Lung Water Volume in Stable Hemodialysis PatientsASAIO Journal, Vol. 52, No. 4Pulmonary Oedema following Exercise in HumansSports Medicine, Vol. 36, No. 6The effect of sustained heavy exercise on the development of pulmonary edema in trained male cyclistsRespiratory Physiology & Neurobiology, Vol. 145, No. 2-3Pulmonary Oedema of ImmersionSports Medicine, Vol. 35, No. 3Intrabreath Diffusing Capacity of the Lung in Healthy Individuals at Rest and During ExerciseChest, Vol. 122, No. 1Extravascular lung water in the exercising horseP. A. Wilkins, R. D. Gleed, N. M. Krivitski, and A. Dobson1 December 2001 | Journal of Applied Physiology, Vol. 91, No. 6Expiratory flow limitation as a determinant of orthopnea in acute left heart failureJournal of the American College of Cardiology, Vol. 35, No. 3Effects of lower body pressure changes on pulmonary functionMedicine & Science in Sports & Exercise, Vol. 30, No. 7Normal Values for Single Exhalation Diffusing Capacity and Pulmonary Capillary Blood Flow in Sitting, Supine Positions, and During Mild ExerciseChest, Vol. 105, No. 2Pulmonary gas exchange and breathing pattern during and after exercise in highly trained athletesEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 67, No. 5Clinical relevance of lung water measurement with the thermal-dye dilution techniqueJournal of Surgical Research, Vol. 48, No. 3Clinical Relevance of Lung Water Measurement with the Thermal-Dye Dilution TechniqueEvaluation of Endothelial Injury in the Human LungClinics in Chest Medicine, Vol. 10, No. 1Determinants of diagnostic accuracy in pulmonary scintigraphy for pulmonary capillary protein leak associated with adult respiratory distress syndrome (ARDS): A technical noteEuropean Journal of Nuclear Medicine, Vol. 15, No. 2Experimental and clinical assessment of lung injury by measurement of extravascular lung water and transcapillary protein flux in ARDS: A review of current techniquesJournal of Surgical Research, Vol. 44, No. 2Lack of Radiographic Evidence of Interstitial Pulmonary Edema after Maximal Exercise in Normal SubjectsAmerican Review of Respiratory Disease, Vol. 137, No. 2Medicion del volumen de tejido y flujo capilar pulmonar mediante tecnicas de dilucion de gases inertes solublesArchivos de Bronconeumología, Vol. 21, No. 5Indirect assessment of thoracic fluid balance following maximal exercise in man14 November 2007 | Journal of Sports Sciences, Vol. 1, No. 3Gram-negative sepsisCurrent Problems in Surgery, Vol. 18, No. 7Gamma camera detection of oleic acid alveolar-capillary albumin leakJournal of Surgical Research, Vol. 29, No. 1Pulmonary OedemaBritish Journal of Diseases of the Chest, Vol. 74Effect of exercise on dilution estimates of extravascular lung water and on the carbon monoxide diffusing capacity in normal adults.Circulation Research, Vol. 37, No. 3Lung water balance More from this issue > Volume 31Issue 3September 1971Pages 375-9 https://doi.org/10.1152/jappl.1971.31.3.375PubMed4939279History Published online 1 September 1971 Published in print 1 September 1971 Metrics

Pulmonary extravascular and intravascular fluid volumes in resting patients

Pulmonary extravascular and intravascular fluid volumes were measured in 29 patients at rest during cardiac catheterization. Increased extravascular fluid volume was clearly related to increased left atrial and pulmonary arterial pressures. It was not related to flow, resistance or intravascular volume. Extravascular water volumes 3 times “normal” were observed without clinical signs of alveolar pulmonary edema. This probably represents increased interstitial volume or edema. Pulmonary intravascular volume (pulmonary blood volume) was observed to act as a rigid compartment, changing little with intravascular pressure, whereas the extravascular volume was very compliant or distensible. A possible feedback relationship between the pulmonary extravascular and intravascular volumes is discussed. Increases in pulmonary extravascular volume described here correlated well with functional capacity and dyspnea as evaluated by the New York Heart Association classification. Individuals with the greatest extravascular volume were most incapacitated. Chest roentgenograms showing pulmonary congestion and interstitial edema were also related to increased pulmonary extravascular volumes.

Transthoracic electrical impedance s a guide to intravascular overload.

Electrical impedance methods have been used to document the accumulation of fluid in living tissues. Change in transthoracic electrical impedance was studied in dogs during deliberate overinfusion with albumin in normal saline solution. Fall in transthoracic impedance was regularly observed with acute intravascular volume overload. Change in transthoracic impedance was accompanied by elevated cardiac output, fall in peripheral resistance and peripheral and pulmonary arteriovenous shunting. Pulmonary interstitial edema occurred in all animals. Impedance changes occur as the result of increased conductivity due to decreased intrapulmonary aeration (atelectasis) or to increased intrathoracic fluid volume. Relative changes in electrical impedance appear to be as sensitive as central venous pressure in the detection of intrathoracic volume changes.

Hyaline Membrane Disease: II: Lung Lecithin

The lecithin content of lung, together with its surface tension properties, were determined in 34 stillbirths, and 61 neonatal deaths. Lecithin content ranged widely from 1·5 to 18·6% of dry lung tissue. In 24 cases the `palmitic-lecithin9 was also measured; it formed 44-79% of the total lecithins. Since the two were related linearly, changes in palmitic-lecithin could be adequately studied by measuring total lecithins. Lecithin content was negatively correlated with minimum surface tension of lung extract in both fresh stillbirths and neonatal deaths. Cases with hyaline membranes had lung lecithin in the lower range ( After 29 weeks9 gestation, fresh stillbirths and neonatal deaths, other than those with hyaline membranes, had normal lung surfactant. The exception was a small group of infants having immature lungs lacking surfactant, and who survived less than 2½ hours; some of these, it is surmised, would have developed hyaline membranes had they survived longer. This was consistent with the fact that well-formed hyaline membranes were only found in infants that had survived for at least 3 hours. Surfactant deficiency probably develops only after birth (except in very immature infants), and as a consequence of an initial rapid consumption of surfactant to form a lining layer covering the alveolar surface, when a gas-liquid interface is created by aeration of lung. Surfactant deficiency, by promoting interstitial pulmonary oedema, is thought to be the immediate cause of hyaline membrane disease. A scheme for the pathogenesis of hyaline membrane disease is set out. It provides a possible mechanism for the different ways in which surfactant deficiency may arise in immature and mature infants. Cases where hyaline membranes occur with normal surfactant fall into three groups: (1) Cases with hyaline membrane disease that have survived several days, the lungs being in the stage of repair. (2) Cases with massive lung haemorrhage, with severe anaemia from haemolytic disease, or with heart failure; extravasation of oedema fluid or blood may be the common factor in this group. (3) Infants of diabetic mothers.

The Valsalva maneuver as a clinical test for circulatory congestion in chronic uremia.

AbstractForty‐four hemodynamic studies were carried out in 19 patients with chronic renal failure in the azotemic state, as well as 16 studies in 16 surgical patients who did not have renal disease but who exhibited some degree of pulmonary insufficiency. The results show that the hyperdynamic circulatory state associated with both diseases can be differentiated only by the anemia of chronic uremia and the frequent radiological evidence of interstitial pulmonary edema associated with hypervolemia. It is clear from these data that a physician is readily able to ascertain hypervolemia and interstitial pulmonary edema with the ordinary sphygmomanometer at the bedside of a chronically uremic patient. Possible mechanisms of the hemodynamic response to chronic renal failure as ascertained in this study are discussed.

Morphologic criteria of pulmonary edema.

The usual morphologic criterion of alveolar edema is the presence of homogeneous acidophilic material in the air spaces. When interstitial pulmonary edema is present, it is often assumed that alveolar edema is associated even though there may not be any demonstrable proteinaceous material in the air spaces. Findings in rat lungs are described that serve as additional criteria of alveolar edema. These are separations of surface epithelium from the alveolar septum to form blebs and larger clear spaces on the alveolar wall, finally resulting in cast-off membranes completely free in the air spaces.

Plasma histamine levels and cardiovascular effects after compound 48-80.

ArticlePlasma histamine levels and cardiovascular effects after compound 48-80.R E Brashear, J C Ross, and R R MartinR E Brashear, J C Ross, and R R MartinPublished Online:01 Aug 1969https://doi.org/10.1152/jappl.1969.27.2.170MoreSectionsPDF (968 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByPlasma histamine levels following administration of radiographic contrast mediaThe British Journal of Radiology, Vol. 58, No. 695Histamine and interstitial Pulmonary Edema in the DogCirculation Research, Vol. 29, No. 4Histamine Release in the Dog After Leukocyte Lysate InjectionInfection and Immunity, Vol. 4, No. 3Adrenergic Mechanisms in the Effects of Histamine in the Pulmonary Circulation of the CatCirculation Research, Vol. 26, No. 3Histamine release as cause of acute hypotension following rapid colloid infusionNaunyn-Schmiedebergs Archiv f�r Pharmakologie, Vol. 267, No. 5 More from this issue > Volume 27Issue 2August 1969Pages 170-3 https://doi.org/10.1152/jappl.1969.27.2.170PubMed4183679History Published online 1 August 1969 Published in print 1 August 1969 Metrics

The hazard of interstitial pulmonary edema.

The hazard of interstitial pulmonary edema.

Experimental hypoxic pulmonary edema in the rat.

ARTICLESExperimental hypoxic pulmonary edema in the ratT. F. Whayne Jr, and J. W. SeveringhausT. F. Whayne Jr, and J. W. SeveringhausPublished Online:01 Dec 1968https://doi.org/10.1152/jappl.1968.25.6.729MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByStudies on the cell biology of interendothelial cell gapsCristhiaan D. Ochoa, and Troy Stevens1 February 2012 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 302, No. 3Hypoxic Pulmonary VasoconstrictionJ. T. Sylvester, Larissa A. Shimoda, Philip I. Aaronson, and Jeremy P. T. Ward1 January 2012 | Physiological Reviews, Vol. 92, No. 1Mechanism of Alveolar Flooding in Acute Pulmonary Oedema30 May 2008Effect of Altitude on the Heart and the LungsCirculation, Vol. 116, No. 19Physiological aspects of high-altitude pulmonary edemaPeter Bärtsch, Heimo Mairbäurl, Marco Maggiorini, and Erik R. Swenson1 March 2005 | Journal of Applied Physiology, Vol. 98, No. 3Role of Nitric Oxide in the Pathogenesis of Chronic Pulmonary HypertensionVáclav Hampl, and Jan Herget10 January 2000 | Physiological Reviews, Vol. 80, No. 4Triolein-Induced Pulmonary Embolization and Increased Microvascular Permeability in Isolated Perfused Rat LungsThe Journal of Trauma: Injury, Infection, and Critical Care, Vol. 47, No. 1Viral respiratory infection increases susceptibility of young rats to hypoxia-induced pulmonary edemaTodd C. Carpenter, John T. Reeves, and Anthony G. Durmowicz1 March 1998 | Journal of Applied Physiology, Vol. 84, No. 3Selected pulmonary biochemical and hematological changes produced by prolonged hypoxia in the ratExperimental and Molecular Pathology, Vol. 45, No. 3Micropuncture measurement of microvascular pressures in isolated lamb lungs during hypoxia.Circulation Research, Vol. 59, No. 4The Bovine Pulmonary Inflammatory Response: Adjuvant Pneumonitis in Calves26 June 2016 | Veterinary Pathology, Vol. 19, No. 5The pathogenesis of pulmonary edemaProgress in Cardiovascular Diseases, Vol. 23, No. 1Alveolar hypoxia increases lung fluid filtration in unanesthetized newborn lambs.Circulation Research, Vol. 46, No. 1Effects of indomethacin on pulmonary hemodynamics and extravascular lung water in sheep after pulmonary microembolismProstaglandins and Medicine, Vol. 3, No. 2Lung fluid exchange after uneven pulmonary artery obstruction in sheep.Circulation Research, Vol. 43, No. 2Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep.Circulation Research, Vol. 40, No. 3Noncardiogenic Forms of Pulmonary EdemaCirculation, Vol. 46, No. 2Pulmonary EdemaCirculation, Vol. 46, No. 2Histamine and interstitial Pulmonary Edema in the DogCirculation Research, Vol. 29, No. 4Sulfur-containing compounds and tolerance in the prevention of certain metabolic effects of phenylthioureaToxicology and Applied Pharmacology, Vol. 16, No. 3 More from this issue > Volume 25Issue 6December 1968Pages 729-732 Copyright & PermissionsCopyright © 1968 the American Physiological Societyhttps://doi.org/10.1152/jappl.1968.25.6.729PubMed5727200History Published online 1 December 1968 Published in print 1 December 1968 Metrics

Mensuration of the arch of the azygos vein and its application to the study of cardiopulmonary disease.

The normal range and size of the arch of the azygos vein in the standard upright chest film has been variously stated. Felson (4) indicates a maximum dimension of 10 mm. Fleischner and Udis (5), in their excellent article, point out that in their experience the upper limits of normal for the transverse dimension of the arch are 5 mm and, in rare instances, 6 mm. These authors, however, fail to describe their technic for measurement and provide no information concerning possible variation with age and sex. Doyle et al. (2) and Swart (7) do give some statistical data but they used horizontal tomography to visualize the azygos arch. This method is inconvenient and the data obtained cannot be translated to the upright 72-inch postero-anterior chest film because of differing target-film distances and the recognized increase in the width of the azygos arch which occurs with assumption of the supine position. This study was undertaken to provide more easily available, useful data. Method The azygos arch appears as a spindle-shaped shadow in the right tracheobronchial angle and was seen in 56 per cent of the normal patients we surveyed (Fig. 1). In order to determine a normal value, we measured the transverse dimension of the azygos arch in standard chest films of 200 normal men and women between the ages of nineteen and sixty-three years. To standardize our method of measurement, we selected the widest diameter of the vein as measured perpendicularly to the wall of the trachea. Because the tracheal wall blends imperceptibly with the azygos vein, the measurement by necessity includes the tracheal wall (Fig. 2). It's inclusion in the measurement, however, does not introduce a significant error since it should be relatively uniform from subject to subject. Early in the study we discovered that the azygos arch is frequently dilated in pregnant women, so we undertook the same measurement in 100 normal pregnant women as well. The results are shown in Table I. Comment Dilatation of the azygos arch is known to occur in cases of venous congestion including congestive heart failure, right ventricular strain, organic and functional tricuspid insufficiency, pericarditis, both constrictive and with effusion, and obstruction of the superior vena cava above the junction of the azygos vein. Dilatation of the azygos arch has also been described in portal hypertension as a result of collateral flow to the azygos system (1–3, 6) (Fig. 3). We have found that knowledge of the normal dimension of the azygos arch is useful in the differentiation of inflammatory and neoplastic pulmonary infiltration from acute congestive pulmonary interstitial edema. These entities may radiographically resemble one another closely and present a difficult differential diagnosis, particularly when presented without knowledge of prior medical history.

Electrothoracic artificial respiration.

TIFICIAL respiration has become synonymous with the positive pressure respirator. These mechanical devices successfully ventilate patients with acute respiratory failure. However, when artificial ventilation is necessary for an extended time, alterations occur in the tracheobronchial tree and lung parenchyma; these include retained secretions, atelectasis, pneumonitis, and interstitial pulmonary edema. As obstructive or inflammatory lesions develop in the lungs there is an increase in the physiological dead space and the related ventilation requirements. Pontoppidan and co-workers report the ratio of dead space to tidal volume may become so large that no improvement in alveolar ventilation occurs with increased tidal volumes? They also found impaired oxygenation in all their patients. Experience indicates that pulmonary complications contribute significantly to the mortality and morbidity of neurosurgical patients, and that these complications are neither minimized nor avoided by our present ventilation techniques. In our search for an improved ventilation technique we have assumed that, if the normal inspiratory muscles could be electrically driven, the chest cage elevated, and the lung uniformly expanded by negative pressure, some reduction in the high pulmonary complication rate might occur. Little attention was given to electronic driving of the normal neuromuscular apparatus in the work of respiration until the reports by Sarnoff and co-workers in 1948. They demonstrated the feasibility of artificial diaphragmatic respiration by electrical phrenic

Pulmonary circulation in the aged.

Pulmonary circulation in the aged.

Interstitial pulmonary edema. An electron microscopic study of the pathology of staphylococcal enterotoxemia in Rhesus monkeys.

Abstract : Interstitial pulmonary edema was produced in rhesus monkeys by intravenous injections of staphylococcal enterotoxin B, a purified protein toxin. The primary pathologic change, as revealed by electron microscopy, was capillary endothelial cell degeneration and necrosis, with less frequent damage to the endothelium of venules. Secondary phenomena were interstitial hemorrhage and edema and a histiocytic infiltrate. There was striking herniation of capillary endothelium into the vascular lumen which may contribute significantly to decreased pulmonary perfusion in this toxemia.

Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs.

Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs.

Acute interstitial pulmonary edema.

ACUTE INTERSTITIAL PULMONARY EDEMAE. ROBERT HEITZMAN, M.D. and FRED M. ZITER, JR., M.D.Audio Available | Share

The lateral roentgenogram in pulmonary edema.

1. Lateral roentgenograms demonstrate that the edema which appears central on the frontal roentgenogram may, in fact, lie in anterior or posterior segments of any lobe of the lung.2. Interstitial and intra-alveolar pulmonary edema accompany each other in most patients irrespective of the cause.3. There are specific signs of interstitial edema, such as septal lines and peribronchial and perivascular cuffing. but others, such as perihilar haze, can be confused with intra-alveolar edema.4. Although gravity probably plays a part in the distribution of edema, it is difficult to obtain conclusive evidene of this in all cases.5. Pulmonary edema appears to shift easily and rapidly from lobe to lobe and from one lung to the other.

Spontaneous acute toxoplasmosis in a marmoset monkey.

SummaryA spontaneous infection with what appears to be Toxoplasma gondii of an immature Oedipomidas oedipus marmoset is reported. The animal arrived five days prior to death from Colombia and had an overwhelming infection with death due to interstitial pneumonia and pulmonary edema. Organisms identified as Toxoplasma on the basis of morphology and transmissibility to mice were recovered from the carcass and were found in all major organs.