Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow
Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock. Thirty-two...
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| Veröffentlicht in: | Critical care (London, England) England), 2007-01, Vol.11 (6), p.R129-R129, Article R129 |
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| creator | Krejci, Vladimir Hiltebrand, Luzius B Jakob, Stephan M Takala, Jukka Sigurdsson, Gisli H |
| description | Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock.
Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.
In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.
Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow. |
| doi_str_mv | 10.1186/cc6197 |
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Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.
In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.
Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow.</description><identifier>ISSN: 1364-8535</identifier><identifier>EISSN: 1466-609X</identifier><identifier>EISSN: 1364-8535</identifier><identifier>DOI: 10.1186/cc6197</identifier><identifier>PMID: 18078508</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Blood flow ; Care and treatment ; Health aspects ; Kidney - blood supply ; Kidney - drug effects ; Liver - blood supply ; Liver - drug effects ; Liver Circulation - drug effects ; Liver Circulation - physiology ; Pancreas - blood supply ; Pancreas - drug effects ; Regional Blood Flow - drug effects ; Regional Blood Flow - physiology ; Renal Circulation - drug effects ; Renal Circulation - physiology ; Septic shock ; Shock, Septic - metabolism ; Shock, Septic - physiopathology ; Splanchnic Circulation - drug effects ; Splanchnic Circulation - physiology ; Swine ; Vasopressin ; Vasopressins - pharmacology</subject><ispartof>Critical care (London, England), 2007-01, Vol.11 (6), p.R129-R129, Article R129</ispartof><rights>COPYRIGHT 2007 BioMed Central Ltd.</rights><rights>Copyright National Library of Medicine - MEDLINE Abstracts 2007</rights><rights>Copyright © 2007 Krejci et al; licensee BioMed Central Ltd. 2007 Krejci et al; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-afe1e06cc74fc762163eb7bc20d23ecff9adbd57d81c07ce1be8f3e0d9772fec3</citedby><cites>FETCH-LOGICAL-c496t-afe1e06cc74fc762163eb7bc20d23ecff9adbd57d81c07ce1be8f3e0d9772fec3</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/PMC2246226/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246226/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18078508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Krejci, Vladimir</creatorcontrib><creatorcontrib>Hiltebrand, Luzius B</creatorcontrib><creatorcontrib>Jakob, Stephan M</creatorcontrib><creatorcontrib>Takala, Jukka</creatorcontrib><creatorcontrib>Sigurdsson, Gisli H</creatorcontrib><title>Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow</title><title>Critical care (London, England)</title><addtitle>Crit Care</addtitle><description>Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock.
Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.
In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.
Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow.</description><subject>Animals</subject><subject>Blood flow</subject><subject>Care and treatment</subject><subject>Health aspects</subject><subject>Kidney - blood supply</subject><subject>Kidney - drug effects</subject><subject>Liver - blood supply</subject><subject>Liver - drug effects</subject><subject>Liver Circulation - drug effects</subject><subject>Liver Circulation - physiology</subject><subject>Pancreas - blood supply</subject><subject>Pancreas - drug effects</subject><subject>Regional Blood Flow - drug effects</subject><subject>Regional Blood Flow - physiology</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Circulation - physiology</subject><subject>Septic shock</subject><subject>Shock, Septic - metabolism</subject><subject>Shock, Septic - physiopathology</subject><subject>Splanchnic Circulation - drug effects</subject><subject>Splanchnic Circulation - physiology</subject><subject>Swine</subject><subject>Vasopressin</subject><subject>Vasopressins - pharmacology</subject><issn>1364-8535</issn><issn>1466-609X</issn><issn>1364-8535</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUdtqHDEMNaUlSdPkE4LpQ58yiS8zticPhRB6g0AptKVvxiPL2Ulm7Yk929K_j5ddekECCenocMQh5JSzC86NugRQvNfPyBFvlWoU6388r71UbWM62R2Sl6XcM8a1UfKAHHLDtOmYOSJfvruS5oyljJHWLDgvI9CySvBwRTEEhKXQFOnsImR0dXlOM0Y3nVMXPV3hvJ3RYUrJ0zClX6_Ii-Cmgif7eky-vX_39eZjc_v5w6eb69sG2l4tjQvIkSkA3QbQSnAlcdADCOaFRAihd37wnfaGA9OAfEATJDLfay2qKnlM3u54582wRg8Yl-wmO-dx7fJvm9xo_9_EcWXv0k8rRKuEUJXg9Z4gp8cNlsXep02unxXL-67tutZsQRc70J2b0I4xpMoFNTyuR0gRw1jn11yLXsmO83rwZncAOZWSMfxRxJndWmV3VlXg2b_6_8L23sgn2OKQQQ</recordid><startdate>20070101</startdate><enddate>20070101</enddate><creator>Krejci, Vladimir</creator><creator>Hiltebrand, Luzius B</creator><creator>Jakob, Stephan M</creator><creator>Takala, Jukka</creator><creator>Sigurdsson, Gisli H</creator><general>BioMed Central Ltd</general><general>National Library of Medicine - MEDLINE Abstracts</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>K9.</scope><scope>5PM</scope></search><sort><creationdate>20070101</creationdate><title>Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow</title><author>Krejci, Vladimir ; Hiltebrand, Luzius B ; Jakob, Stephan M ; Takala, Jukka ; Sigurdsson, Gisli H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-afe1e06cc74fc762163eb7bc20d23ecff9adbd57d81c07ce1be8f3e0d9772fec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Blood flow</topic><topic>Care and treatment</topic><topic>Health aspects</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Liver - blood supply</topic><topic>Liver - drug effects</topic><topic>Liver Circulation - drug effects</topic><topic>Liver Circulation - physiology</topic><topic>Pancreas - blood supply</topic><topic>Pancreas - drug effects</topic><topic>Regional Blood Flow - drug effects</topic><topic>Regional Blood Flow - physiology</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Circulation - physiology</topic><topic>Septic shock</topic><topic>Shock, Septic - metabolism</topic><topic>Shock, Septic - physiopathology</topic><topic>Splanchnic Circulation - drug effects</topic><topic>Splanchnic Circulation - physiology</topic><topic>Swine</topic><topic>Vasopressin</topic><topic>Vasopressins - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krejci, Vladimir</creatorcontrib><creatorcontrib>Hiltebrand, Luzius B</creatorcontrib><creatorcontrib>Jakob, Stephan M</creatorcontrib><creatorcontrib>Takala, Jukka</creatorcontrib><creatorcontrib>Sigurdsson, Gisli H</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 Health & Medical Complete (Alumni)</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>Krejci, Vladimir</au><au>Hiltebrand, Luzius B</au><au>Jakob, Stephan M</au><au>Takala, Jukka</au><au>Sigurdsson, Gisli H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow</atitle><jtitle>Critical care (London, England)</jtitle><addtitle>Crit Care</addtitle><date>2007-01-01</date><risdate>2007</risdate><volume>11</volume><issue>6</issue><spage>R129</spage><epage>R129</epage><pages>R129-R129</pages><artnum>R129</artnum><issn>1364-8535</issn><eissn>1466-609X</eissn><eissn>1364-8535</eissn><abstract>Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock.
Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.
In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.
Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>18078508</pmid><doi>10.1186/cc6197</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Springer Nature OA/Free Journals; SpringerLink Journals - AutoHoldings |
| subjects | Animals Blood flow Care and treatment Health aspects Kidney - blood supply Kidney - drug effects Liver - blood supply Liver - drug effects Liver Circulation - drug effects Liver Circulation - physiology Pancreas - blood supply Pancreas - drug effects Regional Blood Flow - drug effects Regional Blood Flow - physiology Renal Circulation - drug effects Renal Circulation - physiology Septic shock Shock, Septic - metabolism Shock, Septic - physiopathology Splanchnic Circulation - drug effects Splanchnic Circulation - physiology Swine Vasopressin Vasopressins - pharmacology |
| title | Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow |
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