Evidence of transcellular albumin transport after hemorrhagic shock
Hemorrhagic shock-induced ischemia-reperfusion injury is characterized by an increase in microvascular permeability. This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveo...
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| Veröffentlicht in: | Shock (Augusta, Ga.) Ga.), 2005-06, Vol.23 (6), p.565-570 |
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| creator | CHILDS, Ed W UDOBI, Kahdi F HUNTER, Felicia A DHEVAN, Vijian |
| description | Hemorrhagic shock-induced ischemia-reperfusion injury is characterized by an increase in microvascular permeability. This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveolae) transport mechanism(s) may also play a role after shock. The purpose of our study was to investigate the role of caveolae transport after hemorrhagic shock. After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized Sprague-Dawley rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to determine changes in permeability. Rats received an intravenous injection of fluorescein isothiocyanate-bovine albumin during the control period. The fluorescent light intensity emitted from the fluorescein isothiocyanate-bovine albumin was recorded with digital microscopy within the lumen of the microvasculature and was compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin extravasation. Our results demonstrated a marked increase in albumin leak after hemorrhagic shock that was significantly attenuated with two different inhibitors of transcellular transport, N-ethylmaleimide and methyl-beta-cyclodextrin. These data suggest that caveolae transport plays a significant role in microvascular permeability after hemorrhagic shock. |
| doi_str_mv | 10.1097/01.shk.0000164188.46364.2a |
| format | Article |
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This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveolae) transport mechanism(s) may also play a role after shock. The purpose of our study was to investigate the role of caveolae transport after hemorrhagic shock. After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized Sprague-Dawley rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to determine changes in permeability. Rats received an intravenous injection of fluorescein isothiocyanate-bovine albumin during the control period. The fluorescent light intensity emitted from the fluorescein isothiocyanate-bovine albumin was recorded with digital microscopy within the lumen of the microvasculature and was compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin extravasation. Our results demonstrated a marked increase in albumin leak after hemorrhagic shock that was significantly attenuated with two different inhibitors of transcellular transport, N-ethylmaleimide and methyl-beta-cyclodextrin. These data suggest that caveolae transport plays a significant role in microvascular permeability after hemorrhagic shock.</description><identifier>ISSN: 1073-2322</identifier><identifier>EISSN: 1540-0514</identifier><identifier>DOI: 10.1097/01.shk.0000164188.46364.2a</identifier><identifier>PMID: 15897811</identifier><language>eng</language><publisher>Augusta, GA: BioMedical Press</publisher><subject>Albumins - metabolism ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; beta-Cyclodextrins - pharmacology ; Biological and medical sciences ; Biological Transport ; Blood Pressure ; Capillaries - metabolism ; Capillary Permeability ; Cattle ; Emergency and intensive care: infection, septic shock ; Emergency and intensive care: techniques, logistics ; Ethylmaleimide - pharmacology ; Fluorescein-5-isothiocyanate - pharmacology ; Intensive care medicine ; Intensive care unit. Emergency transport systems. Emergency, hospital ward ; Intestine, Small - metabolism ; Male ; Medical sciences ; Microcirculation ; Rats ; Rats, Sprague-Dawley ; Resuscitation ; Shock, Hemorrhagic - metabolism ; Software ; Splanchnic Circulation ; Time Factors ; Urethane - pharmacology</subject><ispartof>Shock (Augusta, Ga.), 2005-06, Vol.23 (6), p.565-570</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16828617$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15897811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHILDS, Ed W</creatorcontrib><creatorcontrib>UDOBI, Kahdi F</creatorcontrib><creatorcontrib>HUNTER, Felicia A</creatorcontrib><creatorcontrib>DHEVAN, Vijian</creatorcontrib><title>Evidence of transcellular albumin transport after hemorrhagic shock</title><title>Shock (Augusta, Ga.)</title><addtitle>Shock</addtitle><description>Hemorrhagic shock-induced ischemia-reperfusion injury is characterized by an increase in microvascular permeability. This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveolae) transport mechanism(s) may also play a role after shock. The purpose of our study was to investigate the role of caveolae transport after hemorrhagic shock. After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized Sprague-Dawley rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to determine changes in permeability. Rats received an intravenous injection of fluorescein isothiocyanate-bovine albumin during the control period. The fluorescent light intensity emitted from the fluorescein isothiocyanate-bovine albumin was recorded with digital microscopy within the lumen of the microvasculature and was compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin extravasation. Our results demonstrated a marked increase in albumin leak after hemorrhagic shock that was significantly attenuated with two different inhibitors of transcellular transport, N-ethylmaleimide and methyl-beta-cyclodextrin. These data suggest that caveolae transport plays a significant role in microvascular permeability after hemorrhagic shock.</description><subject>Albumins - metabolism</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>beta-Cyclodextrins - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biological Transport</subject><subject>Blood Pressure</subject><subject>Capillaries - metabolism</subject><subject>Capillary Permeability</subject><subject>Cattle</subject><subject>Emergency and intensive care: infection, septic shock</subject><subject>Emergency and intensive care: techniques, logistics</subject><subject>Ethylmaleimide - pharmacology</subject><subject>Fluorescein-5-isothiocyanate - pharmacology</subject><subject>Intensive care medicine</subject><subject>Intensive care unit. Emergency transport systems. Emergency, hospital ward</subject><subject>Intestine, Small - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microcirculation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Resuscitation</subject><subject>Shock, Hemorrhagic - metabolism</subject><subject>Software</subject><subject>Splanchnic Circulation</subject><subject>Time Factors</subject><subject>Urethane - pharmacology</subject><issn>1073-2322</issn><issn>1540-0514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFj0tLw0AUhQdRbK3-BQmCy8R75z1LCfUBBTe6LpPJjIlNmjCTCv57A614Nudy-DjcQ8gdQoFg1ANgkZpdAbNQctS64JJJXlB7RpYoOOQgkJ_PNyiWU0bpglyl9AVAOTPqkixQaKM04pKU6--29nvnsyFkU7T75HzXHTobM9tVh77dH9NxiFNmw-Rj1vh-iLGxn63LUjO43TW5CLZL_ubkK_LxtH4vX_LN2_Nr-bjJR8rMlDvGwNYVM6wWAU1A9MiDFKCdQVFTxYWkQvigVUVpACWd1cFrYYDXQnC2IrfH3vFQ9b7ejrHtbfzZ_q2ZgfsTYJOzXZgfd23656SmWqJiv-g2W48</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>CHILDS, Ed W</creator><creator>UDOBI, Kahdi F</creator><creator>HUNTER, Felicia A</creator><creator>DHEVAN, Vijian</creator><general>BioMedical Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20050601</creationdate><title>Evidence of transcellular albumin transport after hemorrhagic shock</title><author>CHILDS, Ed W ; UDOBI, Kahdi F ; HUNTER, Felicia A ; DHEVAN, Vijian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p239t-c330adb393d5f19f11e14f6508c915d27456255ef87b22f076ca8fe85904d5543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Albumins - metabolism</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>beta-Cyclodextrins - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biological Transport</topic><topic>Blood Pressure</topic><topic>Capillaries - metabolism</topic><topic>Capillary Permeability</topic><topic>Cattle</topic><topic>Emergency and intensive care: infection, septic shock</topic><topic>Emergency and intensive care: techniques, logistics</topic><topic>Ethylmaleimide - pharmacology</topic><topic>Fluorescein-5-isothiocyanate - pharmacology</topic><topic>Intensive care medicine</topic><topic>Intensive care unit. Emergency transport systems. Emergency, hospital ward</topic><topic>Intestine, Small - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microcirculation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Resuscitation</topic><topic>Shock, Hemorrhagic - metabolism</topic><topic>Software</topic><topic>Splanchnic Circulation</topic><topic>Time Factors</topic><topic>Urethane - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHILDS, Ed W</creatorcontrib><creatorcontrib>UDOBI, Kahdi F</creatorcontrib><creatorcontrib>HUNTER, Felicia A</creatorcontrib><creatorcontrib>DHEVAN, Vijian</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Shock (Augusta, Ga.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHILDS, Ed W</au><au>UDOBI, Kahdi F</au><au>HUNTER, Felicia A</au><au>DHEVAN, Vijian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence of transcellular albumin transport after hemorrhagic shock</atitle><jtitle>Shock (Augusta, Ga.)</jtitle><addtitle>Shock</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>23</volume><issue>6</issue><spage>565</spage><epage>570</epage><pages>565-570</pages><issn>1073-2322</issn><eissn>1540-0514</eissn><abstract>Hemorrhagic shock-induced ischemia-reperfusion injury is characterized by an increase in microvascular permeability. This increase in permeability is thought to occur mainly via passive transport through interendothelial cell junctions. However, recent data have suggested that a transcellular (caveolae) transport mechanism(s) may also play a role after shock. The purpose of our study was to investigate the role of caveolae transport after hemorrhagic shock. After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mmHg for 1 h in urethane-anesthetized Sprague-Dawley rats. Mesenteric postcapillary venules in a transilluminated segment of small intestine were examined to determine changes in permeability. Rats received an intravenous injection of fluorescein isothiocyanate-bovine albumin during the control period. The fluorescent light intensity emitted from the fluorescein isothiocyanate-bovine albumin was recorded with digital microscopy within the lumen of the microvasculature and was compared with the intensity of light in the extravascular space. The images were downloaded to a computerized image analysis program that quantitates changes in light intensity. This change in light intensity represents albumin extravasation. Our results demonstrated a marked increase in albumin leak after hemorrhagic shock that was significantly attenuated with two different inhibitors of transcellular transport, N-ethylmaleimide and methyl-beta-cyclodextrin. These data suggest that caveolae transport plays a significant role in microvascular permeability after hemorrhagic shock.</abstract><cop>Augusta, GA</cop><pub>BioMedical Press</pub><pmid>15897811</pmid><doi>10.1097/01.shk.0000164188.46364.2a</doi><tpages>6</tpages></addata></record> |
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| subjects | Albumins - metabolism Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals beta-Cyclodextrins - pharmacology Biological and medical sciences Biological Transport Blood Pressure Capillaries - metabolism Capillary Permeability Cattle Emergency and intensive care: infection, septic shock Emergency and intensive care: techniques, logistics Ethylmaleimide - pharmacology Fluorescein-5-isothiocyanate - pharmacology Intensive care medicine Intensive care unit. Emergency transport systems. Emergency, hospital ward Intestine, Small - metabolism Male Medical sciences Microcirculation Rats Rats, Sprague-Dawley Resuscitation Shock, Hemorrhagic - metabolism Software Splanchnic Circulation Time Factors Urethane - pharmacology |
| title | Evidence of transcellular albumin transport after hemorrhagic shock |
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