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PubMed1974

Local antibody production against the murine toxin of Yersinia pestis in a golf ball-induced granuloma.

The method of Garra and Baygorria, for localized antibody production, has been adapted for obtaining high-titered and monospecific antibodies against the murine toxin of Yersinia pestis. A hollow, perforated plastic golf ball surgically implanted under the skin of rabbits induced the formation of a granuloma. When the murine toxin of Y. pestis was injected directly into the granulomatous cavity, an increased amount of antibody was found in the granuloma fluid as compared with serum or with serum antibody obtained by conventional immunization. The granuloma antibody consisted mainly of immunoglobulin G, probably produced locally by lymphoid cells of the granuloma. The immune granuloma fluid and the granuloma tissue were rich in plasma cells and lymphocytes. The chemical composition of the granuloma fluid indicated that it was a transudate.

Animals↗
PubMed1996

Adenosine deaminase (ADA) isoenzyme analysis in pleural effusions: diagnostic role, and relevance to the origin of increased ADA in tuberculous pleurisy.

The rise in adenosine deaminase (ADA) activity in the pleural fluid of tuberculous pleurisy patients, though used for diagnosis, is of unknown origin. In this work, we determined ADA activity and the activities of 2'-deoxyadenosine deaminase and ADA-2 in 350 patients. We also considered whether the results throw light on the origin of high pleural fluid ADA in tuberculous pleurisy and estimated the diagnostic efficiency of 2'-deoxyadenosine deaminase, ADA-2 and total ADA activities with and without the inclusion of the 2'-deoxyadenosine deaminase/ADA activity ratio in a combined criterion. The 350 pleural effusions were classified by previously established criteria as transudates (60 males/18 females) or as tuberculous (49 males/27 females), neoplastic (50 males/39 females), parapneumonic (36 males/19 females), empyematous (11 males/3 females), or miscellaneous (25 males/13 females) exudates. Total ADA, ADA-2 and 2'-deoxyadenosine deaminase activities were, respectively, 127.5 +/- 2.9, 103 +/- 29.5 and 42.8 +/- 14 U.L-1 in tuberculous exudates. With diagnostic thresholds of 47, 40 and 22 U.L-1 respectively, the sensitivities of ADA, ADA-2 and 2'-deoxyadenosine deaminase for tuberculosis were 100, 100 and 95%; their specificities 91, 96 and 92%; and their efficiencies 93, 97 and 93%, respectively. One hundred and one effusions (all 76 tuberculous, 12 neoplastic, 4 parapneumonic and 9 empyematous exudates) had total ADA levels > 47 U.L-1; of these, 8 neoplastic, 1 parapneumonic and all the tuberculous exudates had a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49. The criterion of simultaneously having ADA > 47 U.L-1, ADA-2 > 40 U.L-1 and a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49 was satisfied by all the tuberculous effusions but only eight others (all neoplastic) (sensitivity 100%, specificity 97%, efficiency 98%). We conclude that: 1) high total ADA activity in tuberculous pleural effusions is due mainly to an increase in ADA-2, and, therefore, originated from the only known source monocytes and macrophages; 2) ADA-2 was a more efficient diagnostic marker of tuberculous pleurisy than total ADA activity, although the difference was not statistically significant; and 3) among effusions with high total ADA the 2'-deoxyadenosine deaminase/ADA activity ratio differentiates tuberculous effusions from empyemas and parapneumonic effusions, but fails to discriminate well between tuberculous and neoplastic effusions.

Adenosine Deaminase↗
PubMed1992

[Pleural amyloidosis: thoracoscopic diagnosis and physiopathological approach].

The authors report a case of pleural amyloidosis presenting as a generalised primary amyloidosis with immunological disturbance, in which the diagnosis was made at thoracoscopy. Bronchopulmonary disease during the course of generalised amyloidosis is frequent, but there are only thirteen cases of histologically proven pleural amyloidosis which have been reported in the literature. Using pleuroscopy the histology obtained enables a pathophysiological approach to this disease, taking account of the cells and enzymes found in the pleura, the inflammatory reactions suggests a local production at the pleura level and this would explain the exudative character of some effusions, although a transudate is most often described and is directly linked to congestive cardiac failure. The deposit of fibrin by occluding the stomas of Wang, explains the failure of the absorptive properties of the pleura and also the recurrent nature of these effusions. The pleural disease is without doubt, under-estimated in generalised amyloidosis and the character of the effusions variable. Most often there are transudates secondary to congestive cardiac failure, although exudates occur as a result of local inflammatory phenomena. Amyloidosis should be remembered as a possible cause of exudative pleurisy.

Aged↗
PubMed1983

Transvascular fluid flux measured from intravascular water concentration changes.

We have measured transvascular water flux in eight canine left lower lobes perfused in a zone 3 of West with indocyanine green-stained plasma. Transvascular flux of water was induced by a step change in the inflow pressure. Assuming the indocyanine green-labeled protein did not significantly cross the capillary membrane in one pass, the rate of transvascular fluid flux could be calculated from the change in outflow-to-inflow concentration of water. The method was validated against gravimetric measurements of water exchange. By comparing our direct measurements of transvascular flux with the time course of lobar weight change, we conclude that following changes in inflow pressure, vascular volume changes occur rapidly and slow changes in lung mass can be accounted for exclusively by water exchange. Our method shows transvascular flux follows a biphasic course, suggesting both a membrane and an interstitial resistance to fluid transudation.

Animals↗
PubMed2002

Estimate of the subepithelial hydrostatic pressure that drives inflammatory transudate into the airway lumen.

Inflammatory diseases of the upper respiratory tract are characterized by flow of plasma filtrate across the epithelium into the airway lumen ("transudation"). Elsewhere, we have proposed that extravasation from microvessels causes edema, and this is associated with elevated subepithelial hydrostatic pressure that drives transudation. To test this hypothesis, we have attempted to block transudation by elevating luminal hydrostatic pressure. We measured the appearance of plasma markers into the lumen of an isolated perfused segment of rat trachea in vivo and found that stimulation of one vagal nerve caused a rapid (half-time approximately 5 min) and nonselective increase in the flow of markers from blood to airway lumen. Leukocyte migration also caused transudation that developed much more slowly (half-time = 2-3 h). In both cases, transudation was blocked by application of luminal hydrostatic pressures. The critical luminal pressure needed to block vagally induced transudation was approximately 4.5 cmH2O, and, to block epithelial transudation induced by leukocyte traffic, it was 3 cmH2O, and we conclude that these are the subepithelial pressures that drive inflammatory transudation into the airway lumen.

Albumins↗
PubMed1987

Analysis of immunoglobulin G antibody responses after administration of live and inactivated influenza A vaccine indicates that nasal wash immunoglobulin G is a transudate from serum.

Following intranasal administration of live influenza A virus vaccine or parenteral inoculation of inactivated influenza virus vaccine, immunoglobulin antibody to the influenza virus hemagglutinin was detected in nasal wash specimens from adult volunteers. Several observations supported the suggestion that this immunoglobulin G hemagglutinin nasal wash antibody appeared to be mainly derived from the serum by a process of passive transudation.

Adult↗
PubMed2006

Angiopoietin-2 levels are elevated in exudative pleural effusions.

OBJECTIVE: To examine the pleural fluid (PF) and serum levels of angiopoietin (Ang)-1, Ang-2, and vascular endothelial growth factor (VEGF) in patients with pleural effusions (PEs). METHODS: One hundred fifteen patients, 16 with transudative PEs due to heart failure and 99 with exudative PEs (malignant, 40; para-pneumonic, 24; tuberculous, 13; miscellaneous etiologies, 22) were included in the study. PF and serum levels of the growth factors were measured using enzyme-linked immunosorbent assay. RESULTS: PF Ang-2 and VEGF levels but not Ang-1 levels were higher (p < 0.001) in exudates than in transudates. PF Ang-2 levels were higher in tuberculous PEs than in PEs of any other etiology and were lower in heart failure PEs than in PEs of any other etiology. The highest PF VEGF levels were observed in patients with malignant and parapneumonic PEs. The lowest PF VEGF levels were observed in patients with transudates. In PEs, Ang-2 levels correlate with VEGF levels (p < 0.001), RBC count (p = 0.002), nucleated cell count (p < 0.001), total protein levels (p < 0.001), and lactate dehydrogenase levels (p < 0.001). PF Ang-1 levels were lower than serum Ang-1 levels both in patients with exudates (p < 0.001) and in those with transudates (p = 0.001). PF Ang-2 levels were higher than serum Ang-2 levels both in patients with exudates (p < 0.001) and in those with transudates (p = 0.045). PF VEGF levels were higher than serum VEGF levels in patients with malignant PEs (p < 0.001) and parapneumonic PEs (p = 0.003), but lower than serum VEGF levels in heart failure PEs (p < 0.001). In patients with tuberculous PEs and exudative PEs of miscellaneous etiology, PF and serum VEGF levels did not differ significantly. CONCLUSION: Ang-2 levels but not Ang-1 levels are elevated in exudative PEs, and they correlate with levels of VEGF and markers of pleural inflammation. It is thus possible that Ang-2 along with VEGF participate in pleural inflammation and the pathogenesis of exudative PEs.

Adult↗
PubMed1985

Anatomy and physiology of the pleural space.

The early development of a coelom, a primitive body cavity, with stretchable mesothelial cells endows the subsequently developed internal organs a great flexibility to expand, retract, and deform. In the pleural cavity, in addition, the lung is maintained in an inflated state by the mechanical coupling between the chest wall and the lung; the mesothelial cells with bush-like elongated microvilli enmesh hyaluronic acid-rich lubricants; both minimize the work of breathing. Normal mesothelial cells are fragile in the air, and their intercellular junctions are narrow but labile. The activated mesothelial cells, on the other hand, are resilient and rich in organelles and enzymes to partake in functions such as fibrinolysis, in order to maintain the patency of the pleural cavity. Fluid and electrolytes permeate freely between normal mesothelial cells; the fluid moves in and out of the pleural cavity following Starling's law, with the endothelium as the main barrier. Transudates in the pleural cavity are formed from alterations of the hydrostatic-osmotic pressure relationship, which normally keeps the pleural cavity dry. More than one factor is usually involved in the formation of exudates. Proteins, particles, and cells in the pleural exudates are removed mainly from the preformed stomas and the lymphatic lacuna present in the lower mediastinum and also in the subcostal region and portions of the diaphragm. This removal of the pleural fluid and particles by the lymphatic route is enhanced by the respiratory movements and is partly responsible for the topographic differences of the pleural pressure. Kampmeier's foci found in the location of the stomas are conglomerates of activated mesothelial and lymphoreticular cells with central capillary and lymphatic vessels. They act like tonsils to impede direct entry of undesirable materials from the pleural cavity into the chest wall and mediastinum.

Animals↗
PubMedDate not supplied

Transudative knee effusions in Milroy's disease.

Two patients, mother and son, with Milroy's disease (chronic hereditary lymphedema) presented with chronic asymptomatic knee effusions. Synovial fluids proved to be transudative in nature. The pathogenesis of knee effusions in Milroy's disease is discussed.

Child↗
PubMed1975

Sterility of intestinal transudate during aortic reconstructive procedures.

In 119 patients undergoing intra-abdominal arterial reconstructions, the small intestines were retained in plastic bags and the fluid that passed from the small intestine into the intestinal bag was cultured for bacteria to search for enteric organisms as a source of prosthesis infection. No enteric organisms were recovered from these 119 cultures. Three cultures did yield bacterial growth; in two cases Staphylococcus epidermidis was found and in one instance S aureus was cultured. Under the conditions of this study, which included intravenous administration of cephalothin sodium preoperatively, intraoperatively, and postoperatively, the small intestinal transudate did not harbor enteric bacteria.

Aorta↗
PubMedDate not supplied

Transudative chylothorax: report of two cases and review of the literature.

Transudative chylothorax is a rare entity that has been associated with a limited range of clinical settings. To date, transudative chylothoraces have been described in only 13 patients, most commonly as a result of hepatic cirrhosis. Recognition of the transudative nature of these effusions is important to avoid unnecessary diagnostic testing and inappropriate management strategies. This report describes the presentation, diagnosis and management of two patients with transudative chylothoraces, and provides a brief review of the relevant literature.

Ascites↗
PubMed2006

Venous arterialization in extralobar pulmonary sequestration associated with fetal hydrops.

BACKGROUND/PURPOSE: Fetal extralobar pulmonary sequestration (EPS) is sometimes complicated by massive pleural effusion (PE) leading to fetal hydrops. The underlying mechanisms as well as the origin of the fluid are not well understood. This study was performed to find a histological hallmark of an EPS with massive PE. We hypothesized that venous obstruction has a role to play in the mechanisms of fluid production by EPS. METHODS: We recently experienced 3 cases of fetal EPS complicated by fetal hydrothorax requiring thoracentesis and eventually thoracoamniotic shunt placement. Total protein content and cell count were measured in the aspirates, which were compared with chylothorax cases (n = 5) requiring fetal shunt placement. After birth, all 3 infants required mass resection for the control of PE. The venous wall thickness was measured on pathology slides stained with Elastica van Gieson staining. Thickness of the media and adventitia was measured in approximately 40 veins per case. They were corrected by external diameter and expressed as percentage of medial thickness and percentage of adventitial thickness. An EPS not associated with PE but with congenital diaphragmatic hernia served as a control. RESULTS: Total protein and the cell count of the EPS related PE were 0.6 +/- 0.3 mg/dL and 28 +/- 14/microL (mean +/- SD), which were significantly lower than those of PE in chylothorax (2.2 +/- 0.2 mg/dL and 1900 +/- 1100/microL). Percentages of adventitial thickness of EPS with PE were 9.8% +/- 3.8%, 10.4% +/- 3.6%, and 8.3% +/- 3.7%, which were significantly increased compared with the control of 3.1% +/- 1.3% (P < .01). Percentages of medial thickness of EPS with PE were 7.0% +/- 1.9%, 7.3% +/- 1.4%, and 6.6% +/- 2.3%, which were significantly increased compared with the control of 2.3% +/- 0.7% (P < .01). CONCLUSIONS: We conclude that PE associated with EPS is the transudate rather than the lymph. The thickened media and the adventitia found in EPS with PE support the hypothesis that partial obstruction of the venous system leads to an increased transudate production, which ultimately leads to fetal hydrops.

Bronchopulmonary Sequestration↗
PubMedDate not supplied

The oxygen tension in transudate of the middle ear.

The pO2 of transudate in the middle ear was measured in situ by a small pO2-electrode introduced through the tympanic membrane. Errors involved in some previous methods using aspiration of gas from the middle ear were avoided by the present method since contamination by air from outside of the drum was almost completely eliminated. Seventeen patients, of whom the majority had a naso-pharyngeal carcinoma or chronic otosalpingitis, were investigated. The mean pO2 of the middle ear transudate was 46 mmHg or 6.5% with a pO2 range between 10 and 108 mmHg. Investigations of the function of the Eustachian tube by the aspiration-deflation method after application of a transmyringeal tube was performed in 10 of the patients, revealing no passage through the Eustachian tube. Among these 10 patients only 4 had a passage of air on Politzer, and these had a higher pO2 in the middle ear transudate than the remaining 6 patients in whom Politzer was performed with a negative result.

Adult↗