Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice
Mechanical ventilation can paradoxically cause acute lung injury, which is termed ventilator-induced lung injury. Neutrophil recruitment and neutrophil elastase release play a central role in the pathogenesis of ventilator-induced lung injury including cell damage, extracellular matrix degradation a...
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| Veröffentlicht in: | European journal of pharmacology 2007-09, Vol.571 (1), p.62-71 |
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| creator | Sakashita, Akihiro Nishimura, Yoshihiro Nishiuma, Teruaki Takenaka, Kaori Kobayashi, Kazuyuki Kotani, Yoshikazu Yokoyama, Mitsuhiro |
| description | Mechanical ventilation can paradoxically cause acute lung injury, which is termed ventilator-induced lung injury. Neutrophil recruitment and neutrophil elastase release play a central role in the pathogenesis of ventilator-induced lung injury including cell damage, extracellular matrix degradation and alveolar-capillary hyperpermeability. We therefore speculated that neutrophil elastase inhibition ameliorates ventilator-induced lung injury. Anesthetized C57/BL6 mice received mechanical ventilation with a high tidal volume (V
T; 20 ml/kg) for 4 h. The neutrophil elastase inhibitor (sivelestat, 100 mg/kg) or saline was given intraperitoneally (i.p.) 30 min before ventilation. Sivelestat completely inhibited both neutrophil elastase and myeloperoxidase activities that were increased by ventilation, and attenuated the histopathological degree of lung damage, neutrophil accumulation and lung water content, as well as the concentration of macrophage inflammatory protein (MIP)-2, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid and serum. Moreover, mechanical ventilation increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the expression of early growth response gene-1 (Egr-1) mRNA, and these increases were also recovered by sivelestat. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed apoptotic cells mainly in alveolar epithelial cells and their numbers corresponded to histological damage. These data suggested that sivelestat could protect against ventilator-induced lung injury by suppressing apoptotic responses through mechanical stress-induced cell signaling in addition to inhibiting neutrophil chemotaxis. |
| doi_str_mv | 10.1016/j.ejphar.2007.05.053 |
| format | Article |
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T; 20 ml/kg) for 4 h. The neutrophil elastase inhibitor (sivelestat, 100 mg/kg) or saline was given intraperitoneally (i.p.) 30 min before ventilation. Sivelestat completely inhibited both neutrophil elastase and myeloperoxidase activities that were increased by ventilation, and attenuated the histopathological degree of lung damage, neutrophil accumulation and lung water content, as well as the concentration of macrophage inflammatory protein (MIP)-2, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid and serum. Moreover, mechanical ventilation increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the expression of early growth response gene-1 (Egr-1) mRNA, and these increases were also recovered by sivelestat. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed apoptotic cells mainly in alveolar epithelial cells and their numbers corresponded to histological damage. These data suggested that sivelestat could protect against ventilator-induced lung injury by suppressing apoptotic responses through mechanical stress-induced cell signaling in addition to inhibiting neutrophil chemotaxis.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2007.05.053</identifier><identifier>PMID: 17599828</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject><![CDATA[Acute lung injury ; Animals ; Apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; Blotting, Western ; Bronchoalveolar Lavage Fluid - chemistry ; Chemokine CXCL2 ; Chemokines, CXC - blood ; Chemokines, CXC - metabolism ; Enzyme-Linked Immunosorbent Assay ; Glycine - administration & dosage ; Glycine - analogs & derivatives ; Glycine - pharmacology ; Injections, Intraperitoneal ; Interleukin-6 - blood ; Interleukin-6 - metabolism ; Leukocyte Elastase - antagonists & inhibitors ; Leukocyte Elastase - metabolism ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung Diseases - etiology ; Lung Diseases - metabolism ; Lung Diseases - prevention & control ; Mechanical ventilation ; Mechanotransduction ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases - metabolism ; Neutrophil elastase ; Neutrophil Infiltration - drug effects ; Neutrophils - drug effects ; Neutrophils - pathology ; Pharmacology. Drug treatments ; Pneumology ; Pulmonary Edema - etiology ; Pulmonary Edema - prevention & control ; Respiratory system : syndromes and miscellaneous diseases ; Serine Proteinase Inhibitors - administration & dosage ; Serine Proteinase Inhibitors - pharmacology ; Sivelestat ; Sulfonamides - administration & dosage ; Sulfonamides - pharmacology ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - metabolism ; Ventilators, Mechanical - adverse effects]]></subject><ispartof>European journal of pharmacology, 2007-09, Vol.571 (1), p.62-71</ispartof><rights>2007 Elsevier B.V.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-acadaa411119709036095c713cd769e35f836ff92079eb772ba7bda573d786643</citedby><cites>FETCH-LOGICAL-c434t-acadaa411119709036095c713cd769e35f836ff92079eb772ba7bda573d786643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014299907006401$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19013268$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17599828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sakashita, Akihiro</creatorcontrib><creatorcontrib>Nishimura, Yoshihiro</creatorcontrib><creatorcontrib>Nishiuma, Teruaki</creatorcontrib><creatorcontrib>Takenaka, Kaori</creatorcontrib><creatorcontrib>Kobayashi, Kazuyuki</creatorcontrib><creatorcontrib>Kotani, Yoshikazu</creatorcontrib><creatorcontrib>Yokoyama, Mitsuhiro</creatorcontrib><title>Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Mechanical ventilation can paradoxically cause acute lung injury, which is termed ventilator-induced lung injury. Neutrophil recruitment and neutrophil elastase release play a central role in the pathogenesis of ventilator-induced lung injury including cell damage, extracellular matrix degradation and alveolar-capillary hyperpermeability. We therefore speculated that neutrophil elastase inhibition ameliorates ventilator-induced lung injury. Anesthetized C57/BL6 mice received mechanical ventilation with a high tidal volume (V
T; 20 ml/kg) for 4 h. The neutrophil elastase inhibitor (sivelestat, 100 mg/kg) or saline was given intraperitoneally (i.p.) 30 min before ventilation. Sivelestat completely inhibited both neutrophil elastase and myeloperoxidase activities that were increased by ventilation, and attenuated the histopathological degree of lung damage, neutrophil accumulation and lung water content, as well as the concentration of macrophage inflammatory protein (MIP)-2, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid and serum. Moreover, mechanical ventilation increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the expression of early growth response gene-1 (Egr-1) mRNA, and these increases were also recovered by sivelestat. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed apoptotic cells mainly in alveolar epithelial cells and their numbers corresponded to histological damage. These data suggested that sivelestat could protect against ventilator-induced lung injury by suppressing apoptotic responses through mechanical stress-induced cell signaling in addition to inhibiting neutrophil chemotaxis.</description><subject>Acute lung injury</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Chemokine CXCL2</subject><subject>Chemokines, CXC - blood</subject><subject>Chemokines, CXC - metabolism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Glycine - administration & dosage</subject><subject>Glycine - analogs & derivatives</subject><subject>Glycine - pharmacology</subject><subject>Injections, Intraperitoneal</subject><subject>Interleukin-6 - blood</subject><subject>Interleukin-6 - metabolism</subject><subject>Leukocyte Elastase - antagonists & inhibitors</subject><subject>Leukocyte Elastase - metabolism</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung Diseases - etiology</subject><subject>Lung Diseases - metabolism</subject><subject>Lung Diseases - prevention & control</subject><subject>Mechanical ventilation</subject><subject>Mechanotransduction</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Neutrophil elastase</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pneumology</subject><subject>Pulmonary Edema - etiology</subject><subject>Pulmonary Edema - prevention & control</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>Serine Proteinase Inhibitors - administration & dosage</subject><subject>Serine Proteinase Inhibitors - pharmacology</subject><subject>Sivelestat</subject><subject>Sulfonamides - administration & dosage</subject><subject>Sulfonamides - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Ventilators, Mechanical - adverse effects</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoMo7uzqPxDpi6KHHitJd6dzEWRxVVj0oudQna7eSZPpHvMxsP_eDDOwN0ORguKpl-Jh7A2HLQfefZq3NB92GLYCQG2hLSWfsQ3vla5BcfGcbQB4Uwut9RW7jnEGgFaL9iW74qrVuhf9hj38pJzCetg5X5HHmDBS5ZadG1xaQ_UhuiN5KuP0scKUaMmYKFYxD5H-ZlpSdSyf81jo2i1jtjRWPi8PJWTO4bG0au8svWIvJvSRXl_6Dftz9_X37ff6_te3H7df7mvbyCbVaHFEbHh5WoEG2YFureLSjqrTJNupl900aQFK06CUGFANI7ZKjqrvukbesPfn3ENYy30xmb2LlrzHhdYcTdcLkKqRBWzOoA1rjIEmcwhuj-HRcDAnwWY2Z8HmJNhAW-q09vaSn4c9jU9LF6MFeHcBMFr0U8DFuvjEaeBSdCfu85mjYuPoKJhoHS1FnwtkkxlX9_9L_gHHgZz3</recordid><startdate>20070924</startdate><enddate>20070924</enddate><creator>Sakashita, Akihiro</creator><creator>Nishimura, Yoshihiro</creator><creator>Nishiuma, Teruaki</creator><creator>Takenaka, Kaori</creator><creator>Kobayashi, Kazuyuki</creator><creator>Kotani, Yoshikazu</creator><creator>Yokoyama, Mitsuhiro</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070924</creationdate><title>Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice</title><author>Sakashita, Akihiro ; Nishimura, Yoshihiro ; Nishiuma, Teruaki ; Takenaka, Kaori ; Kobayashi, Kazuyuki ; Kotani, Yoshikazu ; Yokoyama, Mitsuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-acadaa411119709036095c713cd769e35f836ff92079eb772ba7bda573d786643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acute lung injury</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Chemokine CXCL2</topic><topic>Chemokines, CXC - blood</topic><topic>Chemokines, CXC - metabolism</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Glycine - administration & dosage</topic><topic>Glycine - analogs & derivatives</topic><topic>Glycine - pharmacology</topic><topic>Injections, Intraperitoneal</topic><topic>Interleukin-6 - blood</topic><topic>Interleukin-6 - metabolism</topic><topic>Leukocyte Elastase - antagonists & inhibitors</topic><topic>Leukocyte Elastase - metabolism</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung Diseases - etiology</topic><topic>Lung Diseases - metabolism</topic><topic>Lung Diseases - prevention & control</topic><topic>Mechanical ventilation</topic><topic>Mechanotransduction</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Neutrophil elastase</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pneumology</topic><topic>Pulmonary Edema - etiology</topic><topic>Pulmonary Edema - prevention & control</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>Serine Proteinase Inhibitors - administration & dosage</topic><topic>Serine Proteinase Inhibitors - pharmacology</topic><topic>Sivelestat</topic><topic>Sulfonamides - administration & dosage</topic><topic>Sulfonamides - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Ventilators, Mechanical - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sakashita, Akihiro</creatorcontrib><creatorcontrib>Nishimura, Yoshihiro</creatorcontrib><creatorcontrib>Nishiuma, Teruaki</creatorcontrib><creatorcontrib>Takenaka, Kaori</creatorcontrib><creatorcontrib>Kobayashi, Kazuyuki</creatorcontrib><creatorcontrib>Kotani, Yoshikazu</creatorcontrib><creatorcontrib>Yokoyama, Mitsuhiro</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sakashita, Akihiro</au><au>Nishimura, Yoshihiro</au><au>Nishiuma, Teruaki</au><au>Takenaka, Kaori</au><au>Kobayashi, Kazuyuki</au><au>Kotani, Yoshikazu</au><au>Yokoyama, Mitsuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2007-09-24</date><risdate>2007</risdate><volume>571</volume><issue>1</issue><spage>62</spage><epage>71</epage><pages>62-71</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Mechanical ventilation can paradoxically cause acute lung injury, which is termed ventilator-induced lung injury. Neutrophil recruitment and neutrophil elastase release play a central role in the pathogenesis of ventilator-induced lung injury including cell damage, extracellular matrix degradation and alveolar-capillary hyperpermeability. We therefore speculated that neutrophil elastase inhibition ameliorates ventilator-induced lung injury. Anesthetized C57/BL6 mice received mechanical ventilation with a high tidal volume (V
T; 20 ml/kg) for 4 h. The neutrophil elastase inhibitor (sivelestat, 100 mg/kg) or saline was given intraperitoneally (i.p.) 30 min before ventilation. Sivelestat completely inhibited both neutrophil elastase and myeloperoxidase activities that were increased by ventilation, and attenuated the histopathological degree of lung damage, neutrophil accumulation and lung water content, as well as the concentration of macrophage inflammatory protein (MIP)-2, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid and serum. Moreover, mechanical ventilation increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the expression of early growth response gene-1 (Egr-1) mRNA, and these increases were also recovered by sivelestat. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining revealed apoptotic cells mainly in alveolar epithelial cells and their numbers corresponded to histological damage. These data suggested that sivelestat could protect against ventilator-induced lung injury by suppressing apoptotic responses through mechanical stress-induced cell signaling in addition to inhibiting neutrophil chemotaxis.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>17599828</pmid><doi>10.1016/j.ejphar.2007.05.053</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute lung injury Animals Apoptosis Apoptosis - drug effects Biological and medical sciences Blotting, Western Bronchoalveolar Lavage Fluid - chemistry Chemokine CXCL2 Chemokines, CXC - blood Chemokines, CXC - metabolism Enzyme-Linked Immunosorbent Assay Glycine - administration & dosage Glycine - analogs & derivatives Glycine - pharmacology Injections, Intraperitoneal Interleukin-6 - blood Interleukin-6 - metabolism Leukocyte Elastase - antagonists & inhibitors Leukocyte Elastase - metabolism Lung - drug effects Lung - metabolism Lung - pathology Lung Diseases - etiology Lung Diseases - metabolism Lung Diseases - prevention & control Mechanical ventilation Mechanotransduction Medical sciences Mice Mice, Inbred C57BL Mitogen-Activated Protein Kinases - metabolism Neutrophil elastase Neutrophil Infiltration - drug effects Neutrophils - drug effects Neutrophils - pathology Pharmacology. Drug treatments Pneumology Pulmonary Edema - etiology Pulmonary Edema - prevention & control Respiratory system : syndromes and miscellaneous diseases Serine Proteinase Inhibitors - administration & dosage Serine Proteinase Inhibitors - pharmacology Sivelestat Sulfonamides - administration & dosage Sulfonamides - pharmacology Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - metabolism Ventilators, Mechanical - adverse effects |
| title | Neutrophil elastase inhibitor (sivelestat) attenuates subsequent ventilator-induced lung injury in mice |
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