Unilateral radiation pneumonitis in sheep: physiological changes and bronchoalveolar lavage

1989 ◽  
Vol 66 (3) ◽  
pp. 1273-1279 ◽  
Author(s):  
B. F. Tillman ◽  
J. E. Loyd ◽  
A. W. Malcolm ◽  
B. A. Holm ◽  
K. L. Brigham
Keyword(s):  
Pulmonary Hypertension ◽  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Radiation Pneumonitis ◽  
Lower Surface ◽  
Clinical Feature ◽  
Thoracic Irradiation ◽  
Radiation Port ◽  
Lung Irradiation ◽  
Immediate Response

Radiation pneumonitis is a life-threatening result of therapeutic thoracic irradiation, yet its mechanisms are poorly understood. We studied the effects of unilateral lung irradiation (3,000 rad) in sheep from the immediate response to the later development of radiation pneumonitis. We defined radiation pneumonitis by its diagnostic clinical feature, radiographic infiltration of the irradiated zone with a straight margin corresponding to the radiation port. The immediate response in the few hours after irradiation was characterized by cough, labored respiration, hypoxemia (arterial PO2 decreased 19 Torr), mild pulmonary hypertension (pulmonary arterial pressure increased 20%), and lymphopenia. Hemodynamics and gas exchange returned to normal by day 2 but became abnormal again before or during radiation pneumonitis at 32 +/- 2 days. Respiratory distress, hypoxemia, and pulmonary hypertension recurred during radiation pneumonitis. Bronchoalveolar lavage during radiation pneumonitis contained increased neutrophils (19 +/- 4%, control = 7%), increased protein (0.27 +/- 0.1 g/dl, control = 0.12 +/- 0.03), and severely impaired ability to lower surface tension. Alveolar macrophages from both lungs during unilateral radiation pneumonitis exhibited impaired generation of superoxide after phorbol myristate (only a 30% increase). Normal control alveolar macrophages increased superoxide production after stimulation greater than 400%. We conclude that unilateral lung irradiation in sheep causes a mild immediate response followed by radiation pneumonitis at 1 mo. Unilateral radiation pneumonitis in this model is associated with ipsilateral neutrophilic alveolitis, increased bronchoalveolar lavage protein, and impaired surfactant function, as well as bilateral functional abnormalities of alveolar macrophages.

scholarly journals Inducible nitric oxide synthase in pulmonary alveolar macrophages from patients with tuberculosis.

1996 ◽  
Vol 183 (5) ◽  
pp. 2293-2302 ◽  
Author(s):  
S Nicholson ◽  
M da G Bonecini-Almeida ◽  
J R Lapa e Silva ◽  
C Nathan ◽  
Q W Xie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mycobacterium Tuberculosis ◽  
Nitric Oxide Synthase ◽  
Bronchoalveolar Lavage ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Mononuclear Phagocytes ◽  
Mycobacterium Tuberculosis Infection ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The high-output pathway of nitric oxide production helps protect mice from infection by several pathogens, including Mycobacterium tuberculosis. However, based on studies of cells cultured from blood, it is controversial whether human mononuclear phagocytes can express the corresponding inducible nitric oxide synthase (iNOS;NOS2). The present study examined alveolar macrophages fixed directly after bronchopulmonary lavage. An average of 65% of the macrophages from 11 of 11 patients with untreated, culture-positive pulmonary tuberculosis reacted with an antibody documented herein to be monospecific for human NOS2. In contrast, a mean of 10% of bronchoalveolar lavage cells were positive from each of five clinically normal subjects. Tuberculosis patients' macrophages displayed diaphorase activity in the same proportion that they stained for NOS2, under assay conditions wherein the diaphorase reaction was strictly dependent on NOS2 expression. Bronchoalveolar lavage specimens also contained NOS2 mRNA. Thus, macrophages in the lungs of people with clinically active Mycobacterium tuberculosis infection often express catalytically competent NOS2.

scholarly journals Incidence and Correlates of Radiation Pneumonitis in Pediatric Patients With Partial Lung Irradiation

2010 ◽  
Vol 78 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Chiaho Hua ◽  
Kelly A. Hoth ◽  
Shengjie Wu ◽  
Larry E. Kun ◽  
Monika L. Metzger ◽  
...  
Keyword(s):  
Pediatric Patients ◽  
Radiation Pneumonitis ◽  
Lung Irradiation

Modulation by dexamethasone of phospholipase A2 activities in endotoxemic guinea pigs

1995 ◽  
Vol 79 (4) ◽  
pp. 1271-1277 ◽  
Author(s):  
C. M. De Castro ◽  
M. F. Bureau ◽  
M. A. Nahori ◽  
C. H. Dumarey ◽  
B. B. Vargaftig ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Phospholipase A2 ◽  
Alveolar Macrophages ◽  
Guinea Pigs ◽  
Ex Vivo ◽  
Neutrophil Infiltration ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Intracellular Enzyme ◽  
Lps Challenge

One hour after lipopolysaccharide (LPS) administration (intravenous) in guinea pigs, alveolar macrophages are primed for an ex vivo increased secretion of arachidonic acid metabolites from the cyclooxygenase and the lipoxygenase pathways, with challenge by a second stimulus. At the same time, maximal levels of tumor necrosis factor-alpha (TNF-alpha) are observed in the circulation and in the bronchoalveolar lavage fluid. An extracellular form of phospholipase A2, corresponding probably to the low-molecular-mass type II enzyme, known to accumulate in inflammatory exudates, appears later in the serum of guinea pigs, to reach maximal levels 6 h after the LPS. Unlike the intracellular enzyme, extracellular phospholipase A2 is not increased by LPS in alveolar macrophages or in bronchoalveolar lavage fluids. After 24 h, at the time when neither TNF-alpha nor extracellular phospholipase A2 is present and priming of macrophages is over, maximal neutrophil infiltration is observed in the alveolar space of LPS-treated guinea pigs. Dexamethasone administered repeatedly during 3 days (subcutaneous) before the LPS challenge prevented both early events such as the macrophage priming and the TNF-alpha appearance and later events such as extracellular phospholipase A2 release and neutrophil recruitment.

Clinical presentation of pulmonary hypertension

ESC CardioMed ◽  
2018 ◽  
pp. 2495-2497
Author(s):  
Marion Delcroix
Keyword(s):  
Pulmonary Hypertension ◽  
Congenital Heart ◽  
Clinical Presentation ◽  
Heart Diseases ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Right Heart Failure ◽  
Clinical Feature ◽  
Associated Conditions

No clinical feature is pathognomonic for pulmonary hypertension. Signs and symptoms are quite unspecific and can be observed in other lung or heart diseases. This explains why the diagnosis is usually late. Dyspnoea, fatigue, syncope, and angina are the most frequent symptoms. Late in the disease course, signs of right heart failure may also appear, such as hepatomegaly, peripheral oedema, and jugular distension. The clinical presentation is also influenced by the associated conditions, with signs suggestive for systemic sclerosis, portal hypertension, or congenital heart disease. Evaluation of the clinical signs is an important part of patient risk stratification at diagnosis and in the follow-up of patients with pulmonary hypertension.

Localization of a candidate surfactant convertase to type II cells, macrophages, and surfactant subfractions

1999 ◽  
Vol 276 (3) ◽  
pp. L452-L458 ◽  
Author(s):  
Howard Clark ◽  
Lennell Allen ◽  
Erin Collins ◽  
Frederick Barr ◽  
Leland Dobbs ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Pulmonary Surfactant ◽  
Type Ii Cells ◽  
Type Ii ◽  
Clara Cells ◽  
Rat Lung ◽  
Protein Distribution ◽  
Serine Hydrolase ◽  
Surfactant Metabolism

Pulmonary surfactant exists in the alveolus in several distinct subtypes that differ in their morphology, composition, and surface activity. Experiments by others have implicated a serine hydrolase in the production of the inactive small vesicular subtype of surfactant (N. J. Gross and R. M. Schultz. Biochim. Biophys. Acta 1044: 222–230, 1990). Our laboratory recently identified this enzyme in the rat as the serine carboxylesterase ES-2 [F. Barr, H. Clark, and S. Hawgood. Am. J. Physiol. 274 ( Lung Cell. Mol. Physiol. 18): L404–L410, 1998]. In the present study, we determined the cellular sites of expression of ES-2 in rat lung using a digoxygenin-labeled ES-2 riboprobe. ES-2 mRNA was localized to type II cells and alveolar macrophages but not to Clara cells. Using a specific ES-2 antibody, we determined the protein distribution of ES-2 in the lung by immunohistochemistry, and it was found to be consistent with the sites of mRNA expression. Most of the ES-2 in rat bronchoalveolar lavage is in the surfactant-depleted supernatant, but ES-2 was also consistently localized to the small vesicular surfactant subfraction presumed to form as a consequence of conversion activity. These results are consistent with a role for endogenous lung ES-2 in surfactant metabolism.

Determinants of bronchoalveolar lavage cellularity in idiopathic pulmonary fibrosis

1991 ◽  
Vol 71 (5) ◽  
pp. 1688-1693 ◽  
Author(s):  
D. A. Schwartz ◽  
R. A. Helmers ◽  
C. S. Dayton ◽  
R. K. Merchant ◽  
G. W. Hunninghake
Keyword(s):  
Multivariate Analysis ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Cigarette Smoking ◽  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Smoking Status ◽  
Physiological Measures ◽  
Multivariate Models ◽  
Normal Volunteers

To investigate factors that determine bronchoalveolar lavage (BAL) cellularity in patients with idiopathic pulmonary fibrosis (IPF), we compared BAL cells in patients with IPF (n = 83) to both nonsmoking (n = 111) and smoking (n = 19) normal volunteers. Patients with IPF had higher concentrations of BAL total cells and alveolar macrophages than nonsmoking volunteers and more BAL neutrophils and eosinophils than normal volunteers regardless of smoking status. Among patients with IPF, the numbers of alveolar macrophages, neutrophils, or eosinophils were strongly associated with either smoking status or pack-years of cigarette smoking. In fact, after accounting for cigarette smoking, using multivariate analysis, the only additional factors that were found to be associated with BAL cellularity were age (macrophages and eosinophils) and the percent predicted forced expired volume in 1 s (neutrophils). Additional multivariate models failed to identify a significant relationship between BAL cellularity and either the type of immunosuppressive therapy or other physiological measures of lung function. We conclude that cigarette smoking strongly influences BAL cellularity in patients with IPF. These findings suggest that cigarette smoking may have a role in the pathogenesis of IPF or may adversely affect the prognosis in patients with IPF.

scholarly journals Increased leishmanicidal activity of alveolar macrophages from mature horses with mild equine asthma

2019 ◽  
Vol 71 (3) ◽  
pp. 939-943
Author(s):  
D.A.B. Lessa ◽  
N.X. Alencar ◽  
R.A. Torres Filho ◽  
M.F.M. Costa ◽  
W.R. Fernandes ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Phagocytic Activity ◽  
Defense Mechanisms ◽  
Phagocytic Index ◽  
Leishmanicidal Activity ◽  
Phagocytic Ability ◽  
Survival Index ◽  
Mixed Breed ◽  
Equine Asthma

ABSTRACT Alveolar macrophages (AMs) are an essential part of defense mechanisms within the lungs and their phagocytic activity is important for organ homeostasis. The phagocytic ability of AMs obtained from bronchoalveolar lavage from 17 mature mixed-breed pleasure horses (8 healthy and 9 diagnosed with mild equine asthma) was studied through assays with Leishmania (Viannia) braziliensis promastigotes, which enabled the calculation of a phagocytic index (PI) and a survival index (SI). Results indicate that phagocytic activity of AMs in asthma affected horses is similar to healthy horses, while leishmanicidal activity is significantly increased in horses with asthma.

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