Decreased lung hyaluronan in a model of ARDS in the rat: Effect of an inhibitor of leukocyte elastase

Autor:	Chul Min Ahn, Håkan Sandler, Tom Saldeen
Rok vydání:	2012
Předmět:	Male medicine.medical_specialty ARDS Pathology leukocyte elastase inhibitor hyaluronan Rats Sprague-Dawley Extracellular matrix chemistry.chemical_compound Thrombin Internal medicine Hyaluronic acid Acute lung injury medicine Animals pulmonary edema Enzyme Inhibitors Hyaluronic Acid Lung Respiratory Distress Syndrome medicine.diagnostic_test business.industry Original Articles General Medicine acute respiratory distress syndrome respiratory system Pulmonary edema medicine.disease Rats respiratory tract diseases Disease Models Animal Elastase inhibitor Endocrinology medicine.anatomical_structure Bronchoalveolar lavage chemistry Leukocyte Elastase business Bronchoalveolar Lavage Fluid medicine.drug
Zdroj:	Upsala Journal of Medical Sciences
ISSN:	2000-1967 0300-9734
DOI:	10.3109/03009734.2011.622812
Popis:	Background. Hyaluronan (HA) is a component of the extracellular matrix in lung tissue and is normally present at low concentrations in blood. HA is rapidly cleared from blood by the liver. Increased concentrations of plasma HA have been found in patients with acute respiratory distress syndrome (ARDS). We investigated changes in HA levels in plasma, bronchoalveolar lavage fluid (BALF), and lung, and their relationship to pretreatment with a leukocyte elastase inhibitor in a rat model of ARDS. Methods. Rats were randomly assigned to three groups: control, thrombin, and thrombin plus elastase inhibitor. By use of a radiometric assay, HA was measured in lungs, BALF, and plasma. Tissue samples from the lungs were stained for HA and examined microscopically. Liver circulation and cardiac output were monitored using radiolabeled microspheres. Results. Infusion of thrombin produced a pronounced increase in wet weight to dry weight ratio, and relative lung water content. This increase was blunted by a leukocyte elastase inhibitor. A decrease in lung HA and increases in both BALF and plasma HA were found. The leukocyte elastase inhibitor counteracted not only the decrease in lung tissue HA, but also the increase in plasma HA. Histologically, there was decreased HA-staining of peribronchial and perivascular areas in the injured rat lung. Decreased liver perfusion was observed after infusion of thrombin. Conclusions. The decrease in lung HA may be involved in the development of pulmonary edema in this ARDS model, and leukocyte elastase may be one cause of this decrease. In addition, an elevated plasma HA level may be an indicator of lung injury.
Databáze:	OpenAIRE
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