Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats
OBJECTIVETissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models h...
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| Veröffentlicht in: | Critical care medicine 2002-01, Vol.30 (1), p.161-164 |
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| creator | Asakura, Hidesaku Suga, Yukio Aoshima, Keiji Ontachi, Yasuo Mizutani, Tomoe Kato, Minori Saito, Masanori Morishita, Eriko Yamazaki, Masahide Takami, Akiyoshi Miyamoto, Ken-ichi Nakao, Shinji |
| description | OBJECTIVETissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney.
DESIGNProspective, comparative, experimental study.
SETTINGLaboratory at a university hospital.
SUBJECTSTwenty-seven male Wistar rats, age 6–7 wks, weighing 160–170 g.
INTERVENTIONSThree groups of animals were studieda control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein.
MEASUREMENTS AND MAIN RESULTSThe degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration.
CONCLUSIONBecause pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use. |
| doi_str_mv | 10.1097/00003246-200201000-00023 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71531442</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71531442</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4523-e513bd35f0f6301380e0166ecc4811994257cc2c6c76bf849624e03108df80113</originalsourceid><addsrcrecordid>eNp1ksuOVCEQhonROD2jr2DY6O5ocTm3pZl4S8a40TWhOcUcHBqOwLHTb-EjS0_3OCtJCPzJV1VU_RBCGbxlMPbvoC7BZddwAA6sqqZuLp6QDWtFFXwUT8kGYIRGyFFckMucfwIw2fbiOblgbATO235D_nzV6Q4nOjlrMWEwSF2giy5zXOZDdtHH2wPdYtkjBlpczitSq02JqaE6TNS7JS7RH7I2ZtbJTdi4MK3mPmfOuHNBlypcKEn_1tmsXidqor6tl-JioLs4oc_HskmX_II8s9pnfHk-r8iPjx--X39ubr59-nL9_qYxsuWiwZaJ7SRaC7YTwMQACKzr0Bg51O5GWbszhpvO9N3WDnLsuEQQDIbJDsCYuCJvTnmXFH-tmIvauWzQex0wrln1dZBMSl7B4QSaFHNOaNWS3E6ng2Kgjm6oBzfUPzfUvRs19NW5xrrd4fQYeB5_BV6fgToY7W3Swbj8yIn6AMaOnDxx--gLpnzn1z0mNaP2ZVb_-w3iL3P5pAw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71531442</pqid></control><display><type>article</type><title>Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats</title><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>Asakura, Hidesaku ; Suga, Yukio ; Aoshima, Keiji ; Ontachi, Yasuo ; Mizutani, Tomoe ; Kato, Minori ; Saito, Masanori ; Morishita, Eriko ; Yamazaki, Masahide ; Takami, Akiyoshi ; Miyamoto, Ken-ichi ; Nakao, Shinji</creator><creatorcontrib>Asakura, Hidesaku ; Suga, Yukio ; Aoshima, Keiji ; Ontachi, Yasuo ; Mizutani, Tomoe ; Kato, Minori ; Saito, Masanori ; Morishita, Eriko ; Yamazaki, Masahide ; Takami, Akiyoshi ; Miyamoto, Ken-ichi ; Nakao, Shinji</creatorcontrib><description>OBJECTIVETissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney.
DESIGNProspective, comparative, experimental study.
SETTINGLaboratory at a university hospital.
SUBJECTSTwenty-seven male Wistar rats, age 6–7 wks, weighing 160–170 g.
INTERVENTIONSThree groups of animals were studieda control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein.
MEASUREMENTS AND MAIN RESULTSThe degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration.
CONCLUSIONBecause pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.</description><identifier>ISSN: 0090-3493</identifier><identifier>EISSN: 1530-0293</identifier><identifier>DOI: 10.1097/00003246-200201000-00023</identifier><identifier>PMID: 11902257</identifier><identifier>CODEN: CCMDC7</identifier><language>eng</language><publisher>Hagerstown, MD: by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</publisher><subject>Animals ; Antithrombin III ; Biological and medical sciences ; Disease Models, Animal ; Disseminated Intravascular Coagulation - etiology ; Disseminated Intravascular Coagulation - physiopathology ; Fibrin - analysis ; Fibrin Fibrinogen Degradation Products - analysis ; Hematologic and hematopoietic diseases ; Hemostasis - physiology ; Kidney - pathology ; Lipopolysaccharides ; Male ; Medical sciences ; Peptide Hydrolases - blood ; Platelet diseases and coagulopathies ; Prospective Studies ; Rats ; Rats, Wistar ; Thromboplastin</subject><ispartof>Critical care medicine, 2002-01, Vol.30 (1), p.161-164</ispartof><rights>2002 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4523-e513bd35f0f6301380e0166ecc4811994257cc2c6c76bf849624e03108df80113</citedby><cites>FETCH-LOGICAL-c4523-e513bd35f0f6301380e0166ecc4811994257cc2c6c76bf849624e03108df80113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13442117$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11902257$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asakura, Hidesaku</creatorcontrib><creatorcontrib>Suga, Yukio</creatorcontrib><creatorcontrib>Aoshima, Keiji</creatorcontrib><creatorcontrib>Ontachi, Yasuo</creatorcontrib><creatorcontrib>Mizutani, Tomoe</creatorcontrib><creatorcontrib>Kato, Minori</creatorcontrib><creatorcontrib>Saito, Masanori</creatorcontrib><creatorcontrib>Morishita, Eriko</creatorcontrib><creatorcontrib>Yamazaki, Masahide</creatorcontrib><creatorcontrib>Takami, Akiyoshi</creatorcontrib><creatorcontrib>Miyamoto, Ken-ichi</creatorcontrib><creatorcontrib>Nakao, Shinji</creatorcontrib><title>Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats</title><title>Critical care medicine</title><addtitle>Crit Care Med</addtitle><description>OBJECTIVETissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney.
DESIGNProspective, comparative, experimental study.
SETTINGLaboratory at a university hospital.
SUBJECTSTwenty-seven male Wistar rats, age 6–7 wks, weighing 160–170 g.
INTERVENTIONSThree groups of animals were studieda control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein.
MEASUREMENTS AND MAIN RESULTSThe degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration.
CONCLUSIONBecause pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.</description><subject>Animals</subject><subject>Antithrombin III</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Disseminated Intravascular Coagulation - etiology</subject><subject>Disseminated Intravascular Coagulation - physiopathology</subject><subject>Fibrin - analysis</subject><subject>Fibrin Fibrinogen Degradation Products - analysis</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hemostasis - physiology</subject><subject>Kidney - pathology</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Peptide Hydrolases - blood</subject><subject>Platelet diseases and coagulopathies</subject><subject>Prospective Studies</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Thromboplastin</subject><issn>0090-3493</issn><issn>1530-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1ksuOVCEQhonROD2jr2DY6O5ocTm3pZl4S8a40TWhOcUcHBqOwLHTb-EjS0_3OCtJCPzJV1VU_RBCGbxlMPbvoC7BZddwAA6sqqZuLp6QDWtFFXwUT8kGYIRGyFFckMucfwIw2fbiOblgbATO235D_nzV6Q4nOjlrMWEwSF2giy5zXOZDdtHH2wPdYtkjBlpczitSq02JqaE6TNS7JS7RH7I2ZtbJTdi4MK3mPmfOuHNBlypcKEn_1tmsXidqor6tl-JioLs4oc_HskmX_II8s9pnfHk-r8iPjx--X39ubr59-nL9_qYxsuWiwZaJ7SRaC7YTwMQACKzr0Bg51O5GWbszhpvO9N3WDnLsuEQQDIbJDsCYuCJvTnmXFH-tmIvauWzQex0wrln1dZBMSl7B4QSaFHNOaNWS3E6ng2Kgjm6oBzfUPzfUvRs19NW5xrrd4fQYeB5_BV6fgToY7W3Swbj8yIn6AMaOnDxx--gLpnzn1z0mNaP2ZVb_-w3iL3P5pAw</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Asakura, Hidesaku</creator><creator>Suga, Yukio</creator><creator>Aoshima, Keiji</creator><creator>Ontachi, Yasuo</creator><creator>Mizutani, Tomoe</creator><creator>Kato, Minori</creator><creator>Saito, Masanori</creator><creator>Morishita, Eriko</creator><creator>Yamazaki, Masahide</creator><creator>Takami, Akiyoshi</creator><creator>Miyamoto, Ken-ichi</creator><creator>Nakao, Shinji</creator><general>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</general><general>Lippincott</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>200201</creationdate><title>Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats</title><author>Asakura, Hidesaku ; Suga, Yukio ; Aoshima, Keiji ; Ontachi, Yasuo ; Mizutani, Tomoe ; Kato, Minori ; Saito, Masanori ; Morishita, Eriko ; Yamazaki, Masahide ; Takami, Akiyoshi ; Miyamoto, Ken-ichi ; Nakao, Shinji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4523-e513bd35f0f6301380e0166ecc4811994257cc2c6c76bf849624e03108df80113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antithrombin III</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Disseminated Intravascular Coagulation - etiology</topic><topic>Disseminated Intravascular Coagulation - physiopathology</topic><topic>Fibrin - analysis</topic><topic>Fibrin Fibrinogen Degradation Products - analysis</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hemostasis - physiology</topic><topic>Kidney - pathology</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Peptide Hydrolases - blood</topic><topic>Platelet diseases and coagulopathies</topic><topic>Prospective Studies</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Thromboplastin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asakura, Hidesaku</creatorcontrib><creatorcontrib>Suga, Yukio</creatorcontrib><creatorcontrib>Aoshima, Keiji</creatorcontrib><creatorcontrib>Ontachi, Yasuo</creatorcontrib><creatorcontrib>Mizutani, Tomoe</creatorcontrib><creatorcontrib>Kato, Minori</creatorcontrib><creatorcontrib>Saito, Masanori</creatorcontrib><creatorcontrib>Morishita, Eriko</creatorcontrib><creatorcontrib>Yamazaki, Masahide</creatorcontrib><creatorcontrib>Takami, Akiyoshi</creatorcontrib><creatorcontrib>Miyamoto, Ken-ichi</creatorcontrib><creatorcontrib>Nakao, Shinji</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>Critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asakura, Hidesaku</au><au>Suga, Yukio</au><au>Aoshima, Keiji</au><au>Ontachi, Yasuo</au><au>Mizutani, Tomoe</au><au>Kato, Minori</au><au>Saito, Masanori</au><au>Morishita, Eriko</au><au>Yamazaki, Masahide</au><au>Takami, Akiyoshi</au><au>Miyamoto, Ken-ichi</au><au>Nakao, Shinji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats</atitle><jtitle>Critical care medicine</jtitle><addtitle>Crit Care Med</addtitle><date>2002-01</date><risdate>2002</risdate><volume>30</volume><issue>1</issue><spage>161</spage><epage>164</epage><pages>161-164</pages><issn>0090-3493</issn><eissn>1530-0293</eissn><coden>CCMDC7</coden><abstract>OBJECTIVETissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney.
DESIGNProspective, comparative, experimental study.
SETTINGLaboratory at a university hospital.
SUBJECTSTwenty-seven male Wistar rats, age 6–7 wks, weighing 160–170 g.
INTERVENTIONSThree groups of animals were studieda control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein.
MEASUREMENTS AND MAIN RESULTSThe degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration.
CONCLUSIONBecause pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.</abstract><cop>Hagerstown, MD</cop><pub>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</pub><pmid>11902257</pmid><doi>10.1097/00003246-200201000-00023</doi><tpages>4</tpages></addata></record> |
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| subjects | Animals Antithrombin III Biological and medical sciences Disease Models, Animal Disseminated Intravascular Coagulation - etiology Disseminated Intravascular Coagulation - physiopathology Fibrin - analysis Fibrin Fibrinogen Degradation Products - analysis Hematologic and hematopoietic diseases Hemostasis - physiology Kidney - pathology Lipopolysaccharides Male Medical sciences Peptide Hydrolases - blood Platelet diseases and coagulopathies Prospective Studies Rats Rats, Wistar Thromboplastin |
| title | Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats |
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