BIOCHEMICAL ALTERATIONS IN RAT LUNG LAVAGE FLUID FOLLOWING ACUTE SULFUR MUSTARD INHALATION: II. INCREASES IN PROTEOLYTIC ACTIVITY

We have previously shown that mechanical distortion or stretch of alveolar type II (ATII) cells induces both surfactant release and the induction of apoptosis. We hypothesize that nitric oxide (NO) secreted from alveolar macrophages (AMs) prevents cyclic stretch-induced apoptosis. We show that S-nitroso- N-acetyl-d,l-penicillamine (SNAP), a chemical donor of NO, protects cells against nuclear condensation and DNA fragmentation induced by stretch (30% at 60 cycles/min) as well as by sorbitol. SNAP depleted of NO had no protective effect, and the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide blocked the antiapoptotic effect of SNAP. We also show that AMs isolated from rat lung lavage fluid actively synthesize and secrete NO. Using a novel technique in which AMs were cocultured with ATII cells while adhered to floating membrane rafts, we found that NO released from AMs was effective in protecting ATII cells from undergoing apoptosis. We therefore propose that NO secreted by AMs may function as part of a physiological antiapoptotic mechanism that prevents ATII cells from undergoing stretch-induced cell death in the lung.

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Unattenuated Structural and Biochemical Alterations in the Rat Lung during Functional Adaptation to Ozone

American Review of Respiratory Disease ◽

10.1164/ajrccm/140.2.493 ◽

1989 ◽

Vol 140 (2) ◽

pp. 493-501 ◽

Cited By ~ 83

Author(s):

Jeffrey S. Tepper ◽

Daniel L. Costa ◽

James R. Lehmann ◽

Mary F. Weber ◽

Gary E. Hatch

Keyword(s):

Functional Adaptation ◽

Rat Lung ◽

Biochemical Alterations

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The Clinical Clues of Pulmonary Alveolar Proteinosis: A Report of 11 Cases and Literature Review

Canadian Respiratory Journal ◽

10.1155/2016/4021928 ◽

2016 ◽

Vol 2016 ◽

pp. 1-5 ◽

Cited By ~ 1

Author(s):

Qiongya Mo ◽

Bingbin Wang ◽

Nian Dong ◽

Lianmin Bao ◽

Xiaoqiong Su ◽

...

Keyword(s):

Bronchoalveolar Lavage Fluid ◽

Clinical Symptoms ◽

Pulmonary Alveolar Proteinosis ◽

Relevant Literature ◽

Neuron Specific Enolase ◽

Lavage Fluid ◽

Lung Lavage ◽

Serum Markers ◽

Open Lung Biopsy ◽

Alveolar Proteinosis

Pulmonary alveolar proteinosis (PAP) is a rare interstitial lung disease characterized by the abnormal alveolar accumulation of surfactant components. The diagnosis of PAP can be easily missed since it is rare and lacks specific clinical symptoms. It is of great importance to have a better understanding of the crucial clue to clinically diagnose PAP and take PAP into consideration in the differential diagnosis of interstitial pulmonary diseases or other diseases with similar manifestations. Here, we analyze the clinical characteristics of 11 cases of PAP patients in local hospital and review the relevant literature in order to provide more information in diagnosis and management of PAP. In our observation, cyfra21-1 and neuron-specific enolase (NSE) known as tumor markers probably can be useful serum markers for diagnosis of PAP. As for the method of pathologic diagnosis, open-lung biopsy was the gold standard but now it is less required because findings on examination of bronchoalveolar lavage fluid (BALF) can help to make the diagnosis. We also have deep experience about when and how to carry out lung lavage.

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Platelet-activating factor contributes to acute lung leak in rats given interleukin-1 intratracheally

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2000.279.1.l75 ◽

2000 ◽

Vol 279 (1) ◽

pp. L75-L80 ◽

Cited By ~ 29

Author(s):

Young M. Lee ◽

Brooks M. Hybertson ◽

Hyun G. Cho ◽

Lance S. Terada ◽

Okyong Cho ◽

...

Keyword(s):

Interleukin 1 ◽

Platelet Activating Factor ◽

Lavage Fluid ◽

Lung Lavage ◽

Myeloperoxidase Activity ◽

Cerium Chloride ◽

Neutrophil Accumulation ◽

Web 2086

Lung lavage fluid of patients with acute lung injury (ALI) has increased levels of interleukin-1 (IL-1) and neutrophils, but their relationship to the lung leak that characterizes these patients is unclear. To address this concern, we investigated the role of the neutrophil agonist platelet-activating factor [1- O-alkyl-2-acetyl- sn-glycero-3-phosphocholine (PAF)] in the development of the acute neutrophil-dependent lung leak that is induced by giving IL-1 intratracheally to rats. We found that PAF acetyltransferase and PAF activities increased in lungs of rats given IL-1 intratracheally compared with lungs of sham-treated rats given saline intratracheally. The participation of PAF in the development of lung leak and lung neutrophil accumulation after IL-1 administration was suggested when treatment with WEB-2086, a commonly used PAF-receptor antagonist, decreased lung leak, lung myeloperoxidase activity, and lung lavage fluid neutrophil increases in rats given IL-1 intratracheally. Additionally, neutrophils recovered from the lung lavage fluid of rats given IL-1 intratracheally reduced more nitro blue tetrazolium (NBT) in vitro than neutrophils recovered from control rats or rats that had been given WEB-2086 and then IL-1. Histological examination indicated that the endothelial cell-neutrophil interfaces of cerium chloride-stained lung sections of rats given IL-1 contained increased cerium perhydroxide (the reaction product of cerium chloride with hydrogen peroxide) compared with lungs of control rats or rats treated with WEB-2086 and then given IL-1 intratracheally. These in vivo findings were supported by parallel findings showing that WEB-2086 treatment decreased neutrophil adhesion to IL-1-treated cultured endothelial cells in vitro. We concluded that PAF contributes to neutrophil recruitment and neutrophil activation in lungs of rats given IL-1 intratracheally.

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Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1994.266.6.l593 ◽

1994 ◽

Vol 266 (6) ◽

pp. L593-L611 ◽

Cited By ~ 13

Author(s):

M. D. Evans ◽

W. A. Pryor

Keyword(s):

Cigarette Smoke ◽

Proteinase Inhibitor ◽

Inflammatory Cells ◽

Lavage Fluid ◽

Lung Lavage ◽

Tissue Destruction ◽

Phagocytic Cells ◽

Lung Fluid

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.

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