Dual hit lipopolysaccharide & oleic acid combination induced rat model of acute lung injury/acute respiratory distress syndrome
Background & objectives: Despite advances in therapy and overall medical care, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) management remains a problem. Hence the objective of this study was to develop a rat model that mimics human ALI/ARDS. Methods: Four groups of Wistar...
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| Veröffentlicht in: | Indian journal of medical research (New Delhi, India : 1994) India : 1994), 2016-05, Vol.143 (5), p.624-632 |
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| description | Background & objectives: Despite advances in therapy and overall medical care, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) management remains a problem. Hence the objective of this study was to develop a rat model that mimics human ALI/ARDS.
Methods: Four groups of Wistar rats, 48 per group were treated with (i) intratracheal (IT) lipopolysaccharide (LPS) (5 mg/kg) dissolved in normal saline (NS), (ii) intravenous (iv) oleic acid (OA) (250 μl/kg) suspension in bovine serum albumin (BSA), (iii) dual hit: IT LPS (2 mg/kg) dissolved in NS and iv OA (100 μl/kg) and (iv) control group: IT NS and iv BSA. From each group at set periods of time various investigations like chest x-rays, respiratory rate (RR), tidal volume (TV), total cell count, differential cell count, total protein count and cytokine levels in bronchoalveolar lavage fluid (BALF), lung wet/dry weight ratio and histopathological examination were done.
Results: It was noted that the respiratory rate, and tumour necrosis factor-α (TNF-α) levels were significantly higher at 4 h in the dual hit group as compared to LPS, OA and control groups. Interleukin-6 (IL-6) levels were significantly higher in the dual hit group as compared to LPS at 8 and 24 h, OA at 8 h and control (at all time intervals) group. IL-1β levels were significantly higher in LPS and dual hit groups at all time intervals, but not in OA and control groups. The injury induced in dual hit group was earlier and more sustained as compared to LPS and OA alone.
Interpretation & conclusions: The lung pathology and changes in respiration functions produced by the dual hit model were closer to the diagnostic criteria of ALI/ARDS in terms of clinical manifestations and pulmonary injury and the injury persisted longer as compared to LPS and OA single hit model. Therefore, the ARDS model produced by the dual hit method was closer to the diagnostic criteria of ARDS in terms of clinical manifestations and pulmonary injury. |
| doi_str_mv | 10.4103/0971-5916.187111 |
| format | Article |
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Methods: Four groups of Wistar rats, 48 per group were treated with (i) intratracheal (IT) lipopolysaccharide (LPS) (5 mg/kg) dissolved in normal saline (NS), (ii) intravenous (iv) oleic acid (OA) (250 μl/kg) suspension in bovine serum albumin (BSA), (iii) dual hit: IT LPS (2 mg/kg) dissolved in NS and iv OA (100 μl/kg) and (iv) control group: IT NS and iv BSA. From each group at set periods of time various investigations like chest x-rays, respiratory rate (RR), tidal volume (TV), total cell count, differential cell count, total protein count and cytokine levels in bronchoalveolar lavage fluid (BALF), lung wet/dry weight ratio and histopathological examination were done.
Results: It was noted that the respiratory rate, and tumour necrosis factor-α (TNF-α) levels were significantly higher at 4 h in the dual hit group as compared to LPS, OA and control groups. Interleukin-6 (IL-6) levels were significantly higher in the dual hit group as compared to LPS at 8 and 24 h, OA at 8 h and control (at all time intervals) group. IL-1β levels were significantly higher in LPS and dual hit groups at all time intervals, but not in OA and control groups. The injury induced in dual hit group was earlier and more sustained as compared to LPS and OA alone.
Interpretation & conclusions: The lung pathology and changes in respiration functions produced by the dual hit model were closer to the diagnostic criteria of ALI/ARDS in terms of clinical manifestations and pulmonary injury and the injury persisted longer as compared to LPS and OA single hit model. Therefore, the ARDS model produced by the dual hit method was closer to the diagnostic criteria of ARDS in terms of clinical manifestations and pulmonary injury.</description><identifier>ISSN: 0971-5916</identifier><identifier>DOI: 10.4103/0971-5916.187111</identifier><identifier>PMID: 27488006</identifier><language>eng</language><publisher>India: Wolters Kluwer - Medknow Publications</publisher><subject>Acute Lung Injury - chemically induced ; Acute Lung Injury - physiopathology ; Adult respiratory distress syndrome ; Animals ; Bronchoalveolar Lavage Fluid - chemistry ; Causes of ; Disease Models, Animal ; Health aspects ; Humans ; Lipopolysaccharides ; Lipopolysaccharides - toxicity ; Lung - drug effects ; Lung - physiopathology ; Lungs ; Mortality ; Oleic acid ; Oleic Acid - toxicity ; Original ; Pathogenesis ; Rats ; Rats, Wistar ; Respiratory distress syndrome ; Respiratory Distress Syndrome, Adult - chemically induced ; Respiratory Distress Syndrome, Adult - physiopathology ; Rodents ; Tumor necrosis factor-TNF ; Veterinary colleges ; X-rays</subject><ispartof>Indian journal of medical research (New Delhi, India : 1994), 2016-05, Vol.143 (5), p.624-632</ispartof><rights>COPYRIGHT 2016 Medknow Publications and Media Pvt. Ltd.</rights><rights>2016. This work is published under https://creativecommons.org/licenses/by-nc-sa/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright: © Indian Journal of Medical Research 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559y-b6a1d6d5a91450252526e1e1aee6bd4e110158df5998a150eaebcf6b156e4acd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989836/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989836/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27488006$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hagawane, T</creatorcontrib><creatorcontrib>Gaikwad, R</creatorcontrib><creatorcontrib>Kshirsagar, N</creatorcontrib><title>Dual hit lipopolysaccharide & oleic acid combination induced rat model of acute lung injury/acute respiratory distress syndrome</title><title>Indian journal of medical research (New Delhi, India : 1994)</title><addtitle>Indian J Med Res</addtitle><description>Background & objectives: Despite advances in therapy and overall medical care, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) management remains a problem. Hence the objective of this study was to develop a rat model that mimics human ALI/ARDS.
Methods: Four groups of Wistar rats, 48 per group were treated with (i) intratracheal (IT) lipopolysaccharide (LPS) (5 mg/kg) dissolved in normal saline (NS), (ii) intravenous (iv) oleic acid (OA) (250 μl/kg) suspension in bovine serum albumin (BSA), (iii) dual hit: IT LPS (2 mg/kg) dissolved in NS and iv OA (100 μl/kg) and (iv) control group: IT NS and iv BSA. From each group at set periods of time various investigations like chest x-rays, respiratory rate (RR), tidal volume (TV), total cell count, differential cell count, total protein count and cytokine levels in bronchoalveolar lavage fluid (BALF), lung wet/dry weight ratio and histopathological examination were done.
Results: It was noted that the respiratory rate, and tumour necrosis factor-α (TNF-α) levels were significantly higher at 4 h in the dual hit group as compared to LPS, OA and control groups. Interleukin-6 (IL-6) levels were significantly higher in the dual hit group as compared to LPS at 8 and 24 h, OA at 8 h and control (at all time intervals) group. IL-1β levels were significantly higher in LPS and dual hit groups at all time intervals, but not in OA and control groups. The injury induced in dual hit group was earlier and more sustained as compared to LPS and OA alone.
Interpretation & conclusions: The lung pathology and changes in respiration functions produced by the dual hit model were closer to the diagnostic criteria of ALI/ARDS in terms of clinical manifestations and pulmonary injury and the injury persisted longer as compared to LPS and OA single hit model. Therefore, the ARDS model produced by the dual hit method was closer to the diagnostic criteria of ARDS in terms of clinical manifestations and pulmonary injury.</description><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - physiopathology</subject><subject>Adult respiratory distress syndrome</subject><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Causes of</subject><subject>Disease Models, Animal</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung - drug effects</subject><subject>Lung - physiopathology</subject><subject>Lungs</subject><subject>Mortality</subject><subject>Oleic acid</subject><subject>Oleic Acid - toxicity</subject><subject>Original</subject><subject>Pathogenesis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Respiratory distress syndrome</subject><subject>Respiratory Distress Syndrome, Adult - chemically induced</subject><subject>Respiratory Distress Syndrome, Adult - physiopathology</subject><subject>Rodents</subject><subject>Tumor necrosis factor-TNF</subject><subject>Veterinary colleges</subject><subject>X-rays</subject><issn>0971-5916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks1v1DAQxXMA0VK4c0KWkBCX3XqS2IkvSFUpH6ISFzhbjj3Z9daxFzthlRP_er3adtVFyAfLM7_3rLFfUbwBuqyBVpdUNLBgAvgS2gYAnhXnx9JZ8TKlDaUgyka8KM7Kpm5bSvl58ffTpBxZ25E4uw3b4OaktF6raA2S9yQ4tJoobQ3RYeisV6MNnlhvJo2GRDWSIRh0JPSZmkYkbvKr3N9Mcb48VCKmrc1kiDMxNo35nEiavYlhwFfF8165hK8f9ovi1-ebn9dfF7c_vny7vrpdaMbEvOi4AsMNUwJqRkuWF0dAUIi8MzUCUGCt6ZkQrQJGUWGne94B41grbaqL4uPBdzt1AxqNfozKyW20g4qzDMrK0463a7kKf2QtWtFWPBt8eDCI4feEaZSDTRqdUx7DlCS0VHAKDVQZffcPuglT9Hk8WZasLSkv84cdqZVyKK3vQ75X703lVc1EUwnetJla_ofKy-BgdfDY21w_EdCDQMeQUsT-OCNQuQ-K3KdC7lMhD0HJkrdP3-YoeExJBr4fgF1wI8Z056YdRpnZOx92J8aLJ8aSl7Xc50vmfMnHfFX33p_Vpw</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Hagawane, T</creator><creator>Gaikwad, R</creator><creator>Kshirsagar, N</creator><general>Wolters Kluwer - Medknow Publications</general><general>Medknow Publications and Media Pvt. Ltd</general><general>Scientific Scholar</general><general>Medknow Publications & Media Pvt Ltd</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160501</creationdate><title>Dual hit lipopolysaccharide & oleic acid combination induced rat model of acute lung injury/acute respiratory distress syndrome</title><author>Hagawane, T ; Gaikwad, R ; Kshirsagar, N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559y-b6a1d6d5a91450252526e1e1aee6bd4e110158df5998a150eaebcf6b156e4acd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - physiopathology</topic><topic>Adult respiratory distress syndrome</topic><topic>Animals</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Causes of</topic><topic>Disease Models, Animal</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung - drug effects</topic><topic>Lung - physiopathology</topic><topic>Lungs</topic><topic>Mortality</topic><topic>Oleic acid</topic><topic>Oleic Acid - toxicity</topic><topic>Original</topic><topic>Pathogenesis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Respiratory distress syndrome</topic><topic>Respiratory Distress Syndrome, Adult - chemically induced</topic><topic>Respiratory Distress Syndrome, Adult - physiopathology</topic><topic>Rodents</topic><topic>Tumor necrosis factor-TNF</topic><topic>Veterinary colleges</topic><topic>X-rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hagawane, T</creatorcontrib><creatorcontrib>Gaikwad, R</creatorcontrib><creatorcontrib>Kshirsagar, N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hagawane, T</au><au>Gaikwad, R</au><au>Kshirsagar, N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dual hit lipopolysaccharide & oleic acid combination induced rat model of acute lung injury/acute respiratory distress syndrome</atitle><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle><addtitle>Indian J Med Res</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>143</volume><issue>5</issue><spage>624</spage><epage>632</epage><pages>624-632</pages><issn>0971-5916</issn><abstract>Background & objectives: Despite advances in therapy and overall medical care, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) management remains a problem. Hence the objective of this study was to develop a rat model that mimics human ALI/ARDS.
Methods: Four groups of Wistar rats, 48 per group were treated with (i) intratracheal (IT) lipopolysaccharide (LPS) (5 mg/kg) dissolved in normal saline (NS), (ii) intravenous (iv) oleic acid (OA) (250 μl/kg) suspension in bovine serum albumin (BSA), (iii) dual hit: IT LPS (2 mg/kg) dissolved in NS and iv OA (100 μl/kg) and (iv) control group: IT NS and iv BSA. From each group at set periods of time various investigations like chest x-rays, respiratory rate (RR), tidal volume (TV), total cell count, differential cell count, total protein count and cytokine levels in bronchoalveolar lavage fluid (BALF), lung wet/dry weight ratio and histopathological examination were done.
Results: It was noted that the respiratory rate, and tumour necrosis factor-α (TNF-α) levels were significantly higher at 4 h in the dual hit group as compared to LPS, OA and control groups. Interleukin-6 (IL-6) levels were significantly higher in the dual hit group as compared to LPS at 8 and 24 h, OA at 8 h and control (at all time intervals) group. IL-1β levels were significantly higher in LPS and dual hit groups at all time intervals, but not in OA and control groups. The injury induced in dual hit group was earlier and more sustained as compared to LPS and OA alone.
Interpretation & conclusions: The lung pathology and changes in respiration functions produced by the dual hit model were closer to the diagnostic criteria of ALI/ARDS in terms of clinical manifestations and pulmonary injury and the injury persisted longer as compared to LPS and OA single hit model. Therefore, the ARDS model produced by the dual hit method was closer to the diagnostic criteria of ARDS in terms of clinical manifestations and pulmonary injury.</abstract><cop>India</cop><pub>Wolters Kluwer - Medknow Publications</pub><pmid>27488006</pmid><doi>10.4103/0971-5916.187111</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Lung Injury - chemically induced Acute Lung Injury - physiopathology Adult respiratory distress syndrome Animals Bronchoalveolar Lavage Fluid - chemistry Causes of Disease Models, Animal Health aspects Humans Lipopolysaccharides Lipopolysaccharides - toxicity Lung - drug effects Lung - physiopathology Lungs Mortality Oleic acid Oleic Acid - toxicity Original Pathogenesis Rats Rats, Wistar Respiratory distress syndrome Respiratory Distress Syndrome, Adult - chemically induced Respiratory Distress Syndrome, Adult - physiopathology Rodents Tumor necrosis factor-TNF Veterinary colleges X-rays |
| title | Dual hit lipopolysaccharide & oleic acid combination induced rat model of acute lung injury/acute respiratory distress syndrome |
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