Platelet mitochondrial dysfunction in critically ill patients: comparison between sepsis and cardiogenic shock
Platelet mitochondrial respiratory chain enzymes (that produce energy) are variably inhibited during human sepsis. Whether these changes occur even during other acute critical illness or are associated with impaired platelet aggregation and secretion (that consume energy) is not known. The aims of t...
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| creator | Protti, Alessandro Fortunato, Francesco Artoni, Andrea Lecchi, Anna Motta, Giovanna Mistraletti, Giovanni Novembrino, Cristina Comi, Giacomo Pietro Gattinoni, Luciano |
| description | Platelet mitochondrial respiratory chain enzymes (that produce energy) are variably inhibited during human sepsis. Whether these changes occur even during other acute critical illness or are associated with impaired platelet aggregation and secretion (that consume energy) is not known. The aims of this study were firstly to compare platelet mitochondrial respiratory chain enzymes activity between patients with sepsis and those with cardiogenic shock, and secondly to study the relationship between platelet mitochondrial respiratory chain enzymes activity and platelet responsiveness to (exogenous) agonists in patients with sepsis.
This was a prospective, observational, case-control study. Platelets were isolated from venous blood of 16 patients with severe sepsis or septic shock (free from antiplatelet drugs) and 16 others with cardiogenic shock, within 48 hours from admission to Intensive Care. Platelet mitochondrial respiratory chain enzymes activity was measured with spectrophotometry and expressed relative to citrate synthase activity, a marker of mitochondrial density. Platelet aggregation and secretion in response to adenosine di-phosphate (ADP), collagen, U46619 and thrombin receptor activating peptide were measured with lumiaggregometry only in patients with sepsis. In total, 16 healthy volunteers acted as controls for both spectrophotometry and lumiaggregometry.
Platelets of patients with sepsis or cardiogenic shock similarly had lower mitochondrial nicotinamide adenine dinucleotide dehydrogenase (NADH) (P |
| doi_str_mv | 10.1186/s13054-015-0762-7 |
| format | Article |
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This was a prospective, observational, case-control study. Platelets were isolated from venous blood of 16 patients with severe sepsis or septic shock (free from antiplatelet drugs) and 16 others with cardiogenic shock, within 48 hours from admission to Intensive Care. Platelet mitochondrial respiratory chain enzymes activity was measured with spectrophotometry and expressed relative to citrate synthase activity, a marker of mitochondrial density. Platelet aggregation and secretion in response to adenosine di-phosphate (ADP), collagen, U46619 and thrombin receptor activating peptide were measured with lumiaggregometry only in patients with sepsis. In total, 16 healthy volunteers acted as controls for both spectrophotometry and lumiaggregometry.
Platelets of patients with sepsis or cardiogenic shock similarly had lower mitochondrial nicotinamide adenine dinucleotide dehydrogenase (NADH) (P < 0.001), complex I (P = 0.006), complex I and III (P < 0.001) and complex IV (P < 0.001) activity than those of controls. Platelets of patients with sepsis were generally hypo-responsive to exogenous agonists, both in terms of maximal aggregation (P < 0.001) and secretion (P < 0.05). Lower mitochondrial NADH (R (2) 0.36; P < 0.001), complex I (R (2) 0.38; P < 0.001), complex I and III (R (2) 0.27; P = 0.002) and complex IV (R (2) 0.43; P < 0.001) activity was associated with lower first wave of aggregation with ADP.
Several platelet mitochondrial respiratory chain enzymes are similarly inhibited during human sepsis and cardiogenic shock. In patients with sepsis, mitochondrial dysfunction is associated with general platelet hypo-responsiveness to exogenous agonists.
ClinicalTrials.gov NCT00541827 . Registered 8 October 2007.]]></description><identifier>ISSN: 1364-8535</identifier><identifier>EISSN: 1466-609X</identifier><identifier>EISSN: 1364-8535</identifier><identifier>EISSN: 1366-609X</identifier><identifier>DOI: 10.1186/s13054-015-0762-7</identifier><identifier>PMID: 25757508</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Blood platelets ; Blood Platelets - cytology ; Blood Platelets - enzymology ; Cardiogenic shock ; Collagen ; Complications and side effects ; Critical care ; Critical Illness ; Cytochrome ; Data analysis ; Defects ; Electron Transport - physiology ; Electron Transport Chain Complex Proteins - metabolism ; Energy consumption ; Enzymes ; Humans ; Infection ; Metabolism ; Mitochondria ; Mitochondria - enzymology ; Niacinamide ; Phosphates ; Physiological aspects ; Platelet Aggregation - physiology ; Prospective Studies ; Respiration ; Sepsis ; Sepsis - metabolism ; Septic shock ; Shock, Cardiogenic - metabolism ; Thrombin</subject><ispartof>Critical care (London, England), 2015-02, Vol.19 (1), p.39-39, Article 39</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Protti et al.; licensee BioMed Central. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b621t-a3377933f52d32808417cd1fa84ac643bd6a66a0057deaaac78a1357aa6750983</citedby><cites>FETCH-LOGICAL-b621t-a3377933f52d32808417cd1fa84ac643bd6a66a0057deaaac78a1357aa6750983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338849/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338849/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25757508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Protti, Alessandro</creatorcontrib><creatorcontrib>Fortunato, Francesco</creatorcontrib><creatorcontrib>Artoni, Andrea</creatorcontrib><creatorcontrib>Lecchi, Anna</creatorcontrib><creatorcontrib>Motta, Giovanna</creatorcontrib><creatorcontrib>Mistraletti, Giovanni</creatorcontrib><creatorcontrib>Novembrino, Cristina</creatorcontrib><creatorcontrib>Comi, Giacomo Pietro</creatorcontrib><creatorcontrib>Gattinoni, Luciano</creatorcontrib><title>Platelet mitochondrial dysfunction in critically ill patients: comparison between sepsis and cardiogenic shock</title><title>Critical care (London, England)</title><addtitle>Crit Care</addtitle><description><![CDATA[Platelet mitochondrial respiratory chain enzymes (that produce energy) are variably inhibited during human sepsis. Whether these changes occur even during other acute critical illness or are associated with impaired platelet aggregation and secretion (that consume energy) is not known. The aims of this study were firstly to compare platelet mitochondrial respiratory chain enzymes activity between patients with sepsis and those with cardiogenic shock, and secondly to study the relationship between platelet mitochondrial respiratory chain enzymes activity and platelet responsiveness to (exogenous) agonists in patients with sepsis.
This was a prospective, observational, case-control study. Platelets were isolated from venous blood of 16 patients with severe sepsis or septic shock (free from antiplatelet drugs) and 16 others with cardiogenic shock, within 48 hours from admission to Intensive Care. Platelet mitochondrial respiratory chain enzymes activity was measured with spectrophotometry and expressed relative to citrate synthase activity, a marker of mitochondrial density. Platelet aggregation and secretion in response to adenosine di-phosphate (ADP), collagen, U46619 and thrombin receptor activating peptide were measured with lumiaggregometry only in patients with sepsis. In total, 16 healthy volunteers acted as controls for both spectrophotometry and lumiaggregometry.
Platelets of patients with sepsis or cardiogenic shock similarly had lower mitochondrial nicotinamide adenine dinucleotide dehydrogenase (NADH) (P < 0.001), complex I (P = 0.006), complex I and III (P < 0.001) and complex IV (P < 0.001) activity than those of controls. Platelets of patients with sepsis were generally hypo-responsive to exogenous agonists, both in terms of maximal aggregation (P < 0.001) and secretion (P < 0.05). Lower mitochondrial NADH (R (2) 0.36; P < 0.001), complex I (R (2) 0.38; P < 0.001), complex I and III (R (2) 0.27; P = 0.002) and complex IV (R (2) 0.43; P < 0.001) activity was associated with lower first wave of aggregation with ADP.
Several platelet mitochondrial respiratory chain enzymes are similarly inhibited during human sepsis and cardiogenic shock. In patients with sepsis, mitochondrial dysfunction is associated with general platelet hypo-responsiveness to exogenous agonists.
ClinicalTrials.gov NCT00541827 . Registered 8 October 2007.]]></description><subject>Analysis</subject><subject>Blood platelets</subject><subject>Blood Platelets - cytology</subject><subject>Blood Platelets - enzymology</subject><subject>Cardiogenic shock</subject><subject>Collagen</subject><subject>Complications and side effects</subject><subject>Critical care</subject><subject>Critical Illness</subject><subject>Cytochrome</subject><subject>Data analysis</subject><subject>Defects</subject><subject>Electron Transport - physiology</subject><subject>Electron Transport Chain Complex Proteins - metabolism</subject><subject>Energy consumption</subject><subject>Enzymes</subject><subject>Humans</subject><subject>Infection</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - enzymology</subject><subject>Niacinamide</subject><subject>Phosphates</subject><subject>Physiological aspects</subject><subject>Platelet Aggregation - physiology</subject><subject>Prospective Studies</subject><subject>Respiration</subject><subject>Sepsis</subject><subject>Sepsis - metabolism</subject><subject>Septic shock</subject><subject>Shock, Cardiogenic - metabolism</subject><subject>Thrombin</subject><issn>1364-8535</issn><issn>1466-609X</issn><issn>1364-8535</issn><issn>1366-609X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1Uk2LFDEQDaK46-gP8CIBL3vpNel8tgdhWT9hQQ8K3kJ1Oj2TNZ2MSbcy_94Ms66OrNQhIfXeS1W9QugpJeeUavmiUEYEbwgVDVGybdQ9dEq5lI0k3df79c4kb7Rg4gQ9KuWaEKq0ZA_RSStUDaJPUfwUYHbBzXjyc7KbFIfsIeBhV8Yl2tmniH3ENvvZWwhhh30IeAuzd3EuL7FN0xayLxXWu_mncxEXty2-YIgDtpAHn9YueovLJtlvj9GDEUJxT27OFfry9s3ny_fN1cd3Hy4vrppetnRugDGlOsZG0Q6s1URzquxAR9AcrOSsHyRICYQINTgAsEoDZUIByNpWp9kKvTrobpd-coOtxWYIZpv9BHlnEnhznIl-Y9bph-GMac27KvD6IND79B-B40wdhDn4YaofZu-HUVXm7KaOnL4vrsxm8sW6ECC6tBRDpeJSd7yatELP_4FepyXHOiVDO0EFJ1TzP6g1BGd8HFP93e5FzYXgVGiuxF7r_A5UjcFN3qboRl_fjwj0QLA5lZLdeNspJWa_a3f29uzvGd8yfi8X-wUn2tEa</recordid><startdate>20150211</startdate><enddate>20150211</enddate><creator>Protti, Alessandro</creator><creator>Fortunato, Francesco</creator><creator>Artoni, Andrea</creator><creator>Lecchi, Anna</creator><creator>Motta, Giovanna</creator><creator>Mistraletti, Giovanni</creator><creator>Novembrino, Cristina</creator><creator>Comi, Giacomo Pietro</creator><creator>Gattinoni, Luciano</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150211</creationdate><title>Platelet mitochondrial dysfunction in critically ill patients: comparison between sepsis and cardiogenic shock</title><author>Protti, Alessandro ; Fortunato, Francesco ; Artoni, Andrea ; Lecchi, Anna ; Motta, Giovanna ; Mistraletti, Giovanni ; Novembrino, Cristina ; Comi, Giacomo Pietro ; Gattinoni, Luciano</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b621t-a3377933f52d32808417cd1fa84ac643bd6a66a0057deaaac78a1357aa6750983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Blood platelets</topic><topic>Blood Platelets - cytology</topic><topic>Blood Platelets - enzymology</topic><topic>Cardiogenic shock</topic><topic>Collagen</topic><topic>Complications and side effects</topic><topic>Critical care</topic><topic>Critical Illness</topic><topic>Cytochrome</topic><topic>Data analysis</topic><topic>Defects</topic><topic>Electron Transport - physiology</topic><topic>Electron Transport Chain Complex Proteins - metabolism</topic><topic>Energy consumption</topic><topic>Enzymes</topic><topic>Humans</topic><topic>Infection</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - enzymology</topic><topic>Niacinamide</topic><topic>Phosphates</topic><topic>Physiological aspects</topic><topic>Platelet Aggregation - physiology</topic><topic>Prospective Studies</topic><topic>Respiration</topic><topic>Sepsis</topic><topic>Sepsis - metabolism</topic><topic>Septic shock</topic><topic>Shock, Cardiogenic - metabolism</topic><topic>Thrombin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Protti, Alessandro</creatorcontrib><creatorcontrib>Fortunato, Francesco</creatorcontrib><creatorcontrib>Artoni, Andrea</creatorcontrib><creatorcontrib>Lecchi, Anna</creatorcontrib><creatorcontrib>Motta, Giovanna</creatorcontrib><creatorcontrib>Mistraletti, Giovanni</creatorcontrib><creatorcontrib>Novembrino, Cristina</creatorcontrib><creatorcontrib>Comi, Giacomo Pietro</creatorcontrib><creatorcontrib>Gattinoni, Luciano</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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Critical care (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Protti, Alessandro</au><au>Fortunato, Francesco</au><au>Artoni, Andrea</au><au>Lecchi, Anna</au><au>Motta, Giovanna</au><au>Mistraletti, Giovanni</au><au>Novembrino, Cristina</au><au>Comi, Giacomo Pietro</au><au>Gattinoni, Luciano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet mitochondrial dysfunction in critically ill patients: comparison between sepsis and cardiogenic shock</atitle><jtitle>Critical care (London, England)</jtitle><addtitle>Crit Care</addtitle><date>2015-02-11</date><risdate>2015</risdate><volume>19</volume><issue>1</issue><spage>39</spage><epage>39</epage><pages>39-39</pages><artnum>39</artnum><issn>1364-8535</issn><eissn>1466-609X</eissn><eissn>1364-8535</eissn><eissn>1366-609X</eissn><abstract><![CDATA[Platelet mitochondrial respiratory chain enzymes (that produce energy) are variably inhibited during human sepsis. Whether these changes occur even during other acute critical illness or are associated with impaired platelet aggregation and secretion (that consume energy) is not known. The aims of this study were firstly to compare platelet mitochondrial respiratory chain enzymes activity between patients with sepsis and those with cardiogenic shock, and secondly to study the relationship between platelet mitochondrial respiratory chain enzymes activity and platelet responsiveness to (exogenous) agonists in patients with sepsis.
This was a prospective, observational, case-control study. Platelets were isolated from venous blood of 16 patients with severe sepsis or septic shock (free from antiplatelet drugs) and 16 others with cardiogenic shock, within 48 hours from admission to Intensive Care. Platelet mitochondrial respiratory chain enzymes activity was measured with spectrophotometry and expressed relative to citrate synthase activity, a marker of mitochondrial density. Platelet aggregation and secretion in response to adenosine di-phosphate (ADP), collagen, U46619 and thrombin receptor activating peptide were measured with lumiaggregometry only in patients with sepsis. In total, 16 healthy volunteers acted as controls for both spectrophotometry and lumiaggregometry.
Platelets of patients with sepsis or cardiogenic shock similarly had lower mitochondrial nicotinamide adenine dinucleotide dehydrogenase (NADH) (P < 0.001), complex I (P = 0.006), complex I and III (P < 0.001) and complex IV (P < 0.001) activity than those of controls. Platelets of patients with sepsis were generally hypo-responsive to exogenous agonists, both in terms of maximal aggregation (P < 0.001) and secretion (P < 0.05). Lower mitochondrial NADH (R (2) 0.36; P < 0.001), complex I (R (2) 0.38; P < 0.001), complex I and III (R (2) 0.27; P = 0.002) and complex IV (R (2) 0.43; P < 0.001) activity was associated with lower first wave of aggregation with ADP.
Several platelet mitochondrial respiratory chain enzymes are similarly inhibited during human sepsis and cardiogenic shock. In patients with sepsis, mitochondrial dysfunction is associated with general platelet hypo-responsiveness to exogenous agonists.
ClinicalTrials.gov NCT00541827 . Registered 8 October 2007.]]></abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25757508</pmid><doi>10.1186/s13054-015-0762-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; Springer Nature - Complete Springer Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Analysis Blood platelets Blood Platelets - cytology Blood Platelets - enzymology Cardiogenic shock Collagen Complications and side effects Critical care Critical Illness Cytochrome Data analysis Defects Electron Transport - physiology Electron Transport Chain Complex Proteins - metabolism Energy consumption Enzymes Humans Infection Metabolism Mitochondria Mitochondria - enzymology Niacinamide Phosphates Physiological aspects Platelet Aggregation - physiology Prospective Studies Respiration Sepsis Sepsis - metabolism Septic shock Shock, Cardiogenic - metabolism Thrombin |
| title | Platelet mitochondrial dysfunction in critically ill patients: comparison between sepsis and cardiogenic shock |
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