Superoxide production by neutrophils in a model of adult respiratory distress syndrome.

Neutrophils (polymorphonuclear leukocytes [PMNs]) are thought to contribute to the pathophysiology of adult respiratory distress syndrome (ARDS) by the release of toxic oxygen metabolites. This study investigated superoxide production by circulating and bronchoalveolar lavage (BAL) PMNs in a rat model of ARDS induced by chronic Escherichia coli (lipopolysaccharide) endotoxemia. Superoxide production was stimulated by fmet-leu-phe, opsonized zymosan, and phorbol myristate acetate. Circulating and BAL PMNs from lipopolysaccharide-infused rats compared with PMNs from control rats are primed for nonselective increased superoxide production. The BAL PMNs are not only partially primed to release superoxide on adherence, they concomitantly have a depressed superoxide response to a phagocytic (opsonized zymosan) stimulus. These PMN responses may partially explain both the pulmonary injury and the increased susceptibility to pulmonary infection seen in patients with ARDS.

Phenotypic expression of bronchoalveolar lavage cells in lung rejection and infection.

The differentiation of episodes of lung allograft rejection from infection continues to be a problem. Bronchoalveolar lavage (BAL) has recently gained some success in the diagnosis and management of interstitial lung disease. To assess the usefulness of BAL in differentiating between lung allograft rejection and infection, we examined the differences in cellular subsets of BAL and peripheral blood (PBL) samples in a controlled canine model of rejection or pneumonia. Single-lung allotransplants were allowed to undergo rejection by withdrawing immunosuppressive agents (n = 6). In another group of dogs (n = 5), pneumonia was induced by transbronchial injection of Pseudomonas aeruginosa and melted agar followed by bronchial fulguration. Cells obtained from bronchoscopic BAL and PBL samples were labeled with functionally characterized cross-reactive murine monoclonal antibodies. Transthoracic needle biopsies and transbronchial biopsies were done to assess their adequacy in examining the rejecting or infected lungs and were compared with open lung biopsies. We found the following: (1) the percentage of DT2-labeled cells was significantly higher (p less than 0.05) in BAL samples from rejecting lungs compared with infected lungs; (2) the PBL/BAL ratio of DT2-labeled cell percentages was significantly higher in pneumonia (1.7 +/- 0.3) than rejection (0.5 +/- 0.2) (p less than 0.004); (3) the percentage of E11-labeled cells in PBL samples was significantly higher (p less than 0.02) in rejection than in infection; and (4) the ratio of WIG4 to DT2 cellular subset percentages in BAL samples from rejection (26.8 +/- 9.9) was significantly lower than from infection (61.0 +/- 22.9) (p less than 0.03). Transthoracic and transbronchial biopsies did not always yield representative specimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunohistochemical localization of alpha 2-beta 1-glycoprotein in horses.

Alpha 2-beta 1-glycoprotein may be found free in horse serum or complexed with alpha-1-proteinase inhibitor to form pre-alpha 2-elastase inhibitor. There has been little information published concerning alpha 2-beta 1-glycoprotein and its possible tissue sources in horses. A peroxidase-antiperoxidase technique was used to identify alpha 2-beta 1-glycoprotein in buffy coat and bone marrow neutrophils of healthy horses. Macrophages and neutrophils in bronchoalveolar lavage samples from clinically normal horses and from horses with chronic pulmonary disease also were positive for alpha 2-beta 1-glycoprotein. Alpha 2-beta 1-glycoprotein was identified in some instances in normal equine hepatocytes of formalin-fixed liver sections. In formalin-fixed lung sections from horses with chronic, small-airway disease and chronic bronchointerstitial pneumonia, alpha 2-beta 1-glycoprotein was observed in some airway secretions and in macrophages.

[Alpha fetoprotein levels in the serum and bronchoalveolar lavage fluid in patients with lung cancer and other diseases of the respiratory system]. / Stezenie alfa-fetoproteiny w surowicy i materiale z plukania oskrzelowo-pecherzykowego chorych na raka pluca i inne choroby ukladu oddechowego.

Concentration of alpha-fetoprotein (AFP) may be increased in some type of lung cancer. In the study concentration of AFP was evaluated in serum and broncho-alveolar lavage fluid (BALF) in patients with lung cancer. The values of concentration were compared with results obtained from patients with other diseases of the respiratory tract. Examinations were performed in 14 patients with lung cancer, 12 with sarcoidosis, 23 with chronic obstructive bronchitis and 16 with acute bronchitis. Liver pathology was excluded according to biochemical analytical tests. In all patients bronchofibroscopy was performed and BALF was obtained in routine way. Concentration of AFP in serum and BALF was determined by immuno-assay technique. In performed examinations non significant increase of AFP concentration was determined in serum and BALF of patients with lung cancer. However, obtained values were increased twice than in patients with acute bronchitis. Moreover, it was noticed that in patients with chronic obstructive bronchitis the AFP concentration was the highest, especially in the group treated by steroids. The study indicates that evaluation of AFP concentration is out of value in diagnosis and differentiation of lung cancer. It seems to be necessary to continue the examinations for explanation a role of steroids in inflammatory process and increase of AFP concentration.

Vascular changes involved in pulmonary hemorrhage of stroke-prone spontaneously hypertensive rats.

The frequency of pulmonary hemorrhagic lesions in stroke-prone spontaneously hypertensive rats (SHRSP) was higher in older than in younger rats. Hemoglobin and protein contents in pulmonary lavage fluid which may indicate alveolar hemorrhage showed an increase with the progress of age, but the difference of hemorrhagic levels was much more in older rats than that of younger ones. A strong relationship between hemoglobin and protein contents of pulmonary lavage fluid was observed. Morphologically, the most striking feature was fibrinoid degeneration of the vascular walls in the center of hemorrhagic lesions of the lung, not only in the capillaries but also in small arteries. In the early stage of hemorrhage, endothelial discontinuity exhibited intraluminal fibrin deposits in this area of the vessels. Erythrocytes and polygonal deposits of fibrin could also be seen within the same vascular walls. In the advanced stage, subendothelial spaces and medial layers of vascular walls contained an electron-dense amorphous material which was consisted to be a degradation product of fibrinogen. The occurrence of this substance was thought to be induced by the hemodynamic effects of hypertension, the results of increased permeability and the accumulation of blood components. From these results, we suggest that fibrinoid degeneration due to abnormal cellular permeability associated with hypertension in SHRSP may be in some way linked to the development of pulmonary hemorrhage.

Role of pulmonary alveolar macrophage activation in acute lung injury after burns and smoke inhalation.

Bronchoalveolar lavage cells from 42 fire victims and from 18 patients who were smokers attending for diagnostic bronchoscopy (controls) were assessed morphologically and by chemiluminescence. 10 of the victims had inhaled smoke only; 15 had cutaneous burns only; and 17 had combined injury. The combined injury group had significant increases in polymorphonuclear leucocytes and macrophages, especially mature forms, compared with controls. These increases were higher than those expected from the individual injuries. The combined injury group had significantly greater spontaneous chemiluminescence than controls, again greater than that expected by the individual injuries. The chemiluminescence response to stimulation by opsonised bacteria was significantly higher in the combined injury group than in controls, but significantly lower than that in the smoke inhalation only group. The size of the alveolar cellular response to smoke and cutaneous burns suggests that lung damage follows from excess release of inflammatory mediators, exhaustion of the reserve of mature phagocytes and consequent reduced ability to fight bacteria, or both.