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

Hdl Handle:
http://hdl.handle.net/10147/209009
Title:
Attenuation of pancreatitis-induced pulmonary injury by aerosolized hypertonic saline.
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.
Citation:
Surg Infect (Larchmt). 2001 Fall;2(3):215-23; discussion 223-4.
Journal:
Surgical infections
Issue Date:
3-Feb-2012
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
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
ISSN:
1096-2964 (Print); 1096-2964 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorShields, C Jen_GB
dc.contributor.authorSookhai, Sen_GB
dc.contributor.authorWinter, D Cen_GB
dc.contributor.authorDowdall, J Fen_GB
dc.contributor.authorKingston, Gen_GB
dc.contributor.authorParfrey, Nen_GB
dc.contributor.authorWang, J Hen_GB
dc.contributor.authorKirwan, W Oen_GB
dc.contributor.authorRedmond, H Pen_GB
dc.date.accessioned2012-02-03T15:09:48Z-
dc.date.available2012-02-03T15:09:48Z-
dc.date.issued2012-02-03T15:09:48Z-
dc.identifier.citationSurg Infect (Larchmt). 2001 Fall;2(3):215-23; discussion 223-4.en_GB
dc.identifier.issn1096-2964 (Print)en_GB
dc.identifier.issn1096-2964 (Linking)en_GB
dc.identifier.pmid12593711en_GB
dc.identifier.doi10.1089/109629601317202696en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209009-
dc.description.abstractBACKGROUND: 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAcute Diseaseen_GB
dc.subject.meshAdjuvants, Immunologic/*administration & dosage/therapeutic useen_GB
dc.subject.meshAdministration, Inhalationen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshApoptosis/physiologyen_GB
dc.subject.meshBronchoalveolar Lavage Fluid/chemistryen_GB
dc.subject.meshChemotaxis, Leukocyte/physiologyen_GB
dc.subject.meshEndothelial Growth Factors/secretionen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntercellular Signaling Peptides and Proteins/secretionen_GB
dc.subject.meshLung/chemistry/metabolismen_GB
dc.subject.meshLung Diseases/*drug therapy/*etiology/physiopathologyen_GB
dc.subject.meshLymphokines/secretionen_GB
dc.subject.meshMaleen_GB
dc.subject.meshModels, Animalen_GB
dc.subject.meshNeutrophils/physiologyen_GB
dc.subject.meshOrgan Size/drug effectsen_GB
dc.subject.meshPancreatitis/chemically induced/*complicationsen_GB
dc.subject.meshPeroxidase/analysisen_GB
dc.subject.meshProteins/analysisen_GB
dc.subject.meshRatsen_GB
dc.subject.meshRats, Sprague-Dawleyen_GB
dc.subject.meshSaline Solution, Hypertonic/*administration & dosage/therapeutic useen_GB
dc.subject.meshVascular Endothelial Growth Factor Aen_GB
dc.subject.meshVascular Endothelial Growth Factorsen_GB
dc.titleAttenuation of pancreatitis-induced pulmonary injury by aerosolized hypertonic saline.en_GB
dc.contributor.departmentDepartment of Academic Surgery, Cork University Hospital, Wilton, Cork.en_GB
dc.identifier.journalSurgical infectionsen_GB
dc.description.provinceMunster-

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