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    Attenuation of pancreatitis-induced pulmonary injury by aerosolized hypertonic saline.

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    Authors
    Shields, C J
    Sookhai, S
    Winter, D C
    Dowdall, J F
    Kingston, G
    Parfrey, N
    Wang, J H
    Kirwan, W O
    Redmond, H P
    Affiliation
    Department of Academic Surgery, Cork University Hospital, Wilton, Cork.
    Issue Date
    2012-02-03T15:09:48Z
    MeSH
    Acute Disease
    Adjuvants, Immunologic/*administration & dosage/therapeutic use
    Administration, Inhalation
    Animals
    Apoptosis/physiology
    Bronchoalveolar Lavage Fluid/chemistry
    Chemotaxis, Leukocyte/physiology
    Endothelial Growth Factors/secretion
    Humans
    Intercellular Signaling Peptides and Proteins/secretion
    Lung/chemistry/metabolism
    Lung Diseases/*drug therapy/*etiology/physiopathology
    Lymphokines/secretion
    Male
    Models, Animal
    Neutrophils/physiology
    Organ Size/drug effects
    Pancreatitis/chemically induced/*complications
    Peroxidase/analysis
    Proteins/analysis
    Rats
    Rats, Sprague-Dawley
    Saline Solution, Hypertonic/*administration & dosage/therapeutic use
    Vascular Endothelial Growth Factor A
    Vascular Endothelial Growth Factors
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    Citation
    Surg Infect (Larchmt). 2001 Fall;2(3):215-23; discussion 223-4.
    Journal
    Surgical infections
    URI
    http://hdl.handle.net/10147/209009
    DOI
    10.1089/109629601317202696
    PubMed ID
    12593711
    Abstract
    BACKGROUND: The immunomodulatory effects of hypertonic saline (HTS) provide potential strategies to attenuate inappropriate inflammatory reactions. This study tested the hypothesis that administration of intratracheal aerosolized HTS modulates the development of lung injury in pancreatitis. METHODS: Pancreatitis was induced in 24 male Sprague-Dawley rats by intraperitoneal injection of 20% L-arginine (500 mg/100 g body weight). At 24 and 48 h, intratracheal aerosolized HTS (7.5% NaCl, 0.5 mL) was administered to 8 rats, while a further 8 received 0.5 mL of aerosolized normal saline (NS). At 72 hours, pulmonary neutrophil infiltration (myeloperoxidase activity) and endothelial permeability (bronchoalveolar lavage and wet:dry weight ratios) were assessed. In addition, histological assessment of representative lung tissue was performed by a blinded assessor. In a separate experiment, polymorphonucleocytes (PMN) were isolated from human donors, and exposed to increments of HTS. Neutrophil transmigration across an endothelial cell layer, VEGF release, and apoptosis at 1, 6, 12, 18, and 24 h were assessed. RESULTS: Histopathological lung injury scores were significantly reduced in the HTS group (4.78 +/- 1.43 vs. 8.64 +/- 0.86); p < 0.001). Pulmonary neutrophil sequestration (1.40 +/- 0.2) and increased endothelial permeability (6.77 +/- 1.14) were evident in the animals resuscitated with normal saline when compared with HTS (0.70 +/- 0.1 and 3.57 +/- 1.32), respectively; p < 0.04). HTS significantly reduced PMN transmigration (by 97.1, p = 0.002, and induced PMN apoptosis (p < 0.03). HTS did not impact significantly upon neutrophil VEGF release (p > 0.05). CONCLUSIONS: Intratracheal aerosolized HTS attenuates the neutrophil-mediated pulmonary insult subsequent to pancreatitis. This may represent a novel therapeutic strategy.
    Language
    eng
    ISSN
    1096-2964 (Print)
    1096-2964 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1089/109629601317202696
    Scopus Count
    Collections
    Cork University Hospital

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