Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions
1 La Jolla Bioengineering Institute; and 2 Department of Bioengineering, University of California, San Diego, La Jolla, California Submitted 14 April 2006 ; accepted in final form 24 May 2006 The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extre...
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creator | Cabrales, Pedro Tsai, Amy G |
description | 1 La Jolla Bioengineering Institute; and 2 Department of Bioengineering, University of California, San Diego, La Jolla, California
Submitted 14 April 2006
; accepted in final form 24 May 2006
The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extreme hemodilution with low- and high-viscosity plasma expanders (LVPE and HVPE, respectively) to determine whether plasma viscosity is a factor in homeostasis during extreme anemic conditions. Moderated hemodilution was induced by two isovolemic steps performed with 6% 70-kDa dextran until systemic hematocrit (Hct) was reduced to 18% ( level 2 ). In a third isovolemic step, hemodilution with LVPE (6% 70-kDa dextran, 2.8 cP) or HVPE (6% 500-kDa dextran, 5.9 cP) reduced Hct to 11%. Systemic parameters, cardiac output (CO), organ flow distribution, microhemodynamics, and functional capillary density, were measured after each exchange dilution. Fluorescent-labeled microspheres were used to measure organ (brain, heart, kidney, liver, lung, and spleen) and window chamber blood flow. Final blood and plasma viscosities after the entire protocol were 2.1 and 1.4 cP, respectively, for LVPE and 2.8 and 2.2 cP, respectively, for HVPE (baseline = 4.2 and 1.2 cP, respectively). HVPE significantly elevated mean arterial pressure and CO compared with LVPE but did not increase vascular resistance. Functional capillary density was significantly higher for HVPE [87% (SD 7) of baseline] than for LVPE [42% (SD 11) of baseline]. Increases in mean arterial blood pressure, CO, and shear stress-mediated factors could be responsible for maintaining organ and microvascular perfusion after exchange with HVPE compared with LVPE. Microhemodynamic data corresponded to microsphere-measured perfusion data in vital organs.
microcirculation; extreme hemodilution; plasma expander; organ flow distribution; intravascular oxygen; functional capillary density
Address for reprint requests and other correspondence: P. Cabrales, La Jolla Bioengineering Institute, 505 Coast Blvd. South, La Jolla, CA 92037 (e-mail: pcabrales{at}ucsd.edu ) |
doi_str_mv | 10.1152/ajpheart.00394.2006 |
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Submitted 14 April 2006
; accepted in final form 24 May 2006
The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extreme hemodilution with low- and high-viscosity plasma expanders (LVPE and HVPE, respectively) to determine whether plasma viscosity is a factor in homeostasis during extreme anemic conditions. Moderated hemodilution was induced by two isovolemic steps performed with 6% 70-kDa dextran until systemic hematocrit (Hct) was reduced to 18% ( level 2 ). In a third isovolemic step, hemodilution with LVPE (6% 70-kDa dextran, 2.8 cP) or HVPE (6% 500-kDa dextran, 5.9 cP) reduced Hct to 11%. Systemic parameters, cardiac output (CO), organ flow distribution, microhemodynamics, and functional capillary density, were measured after each exchange dilution. Fluorescent-labeled microspheres were used to measure organ (brain, heart, kidney, liver, lung, and spleen) and window chamber blood flow. Final blood and plasma viscosities after the entire protocol were 2.1 and 1.4 cP, respectively, for LVPE and 2.8 and 2.2 cP, respectively, for HVPE (baseline = 4.2 and 1.2 cP, respectively). HVPE significantly elevated mean arterial pressure and CO compared with LVPE but did not increase vascular resistance. Functional capillary density was significantly higher for HVPE [87% (SD 7) of baseline] than for LVPE [42% (SD 11) of baseline]. Increases in mean arterial blood pressure, CO, and shear stress-mediated factors could be responsible for maintaining organ and microvascular perfusion after exchange with HVPE compared with LVPE. Microhemodynamic data corresponded to microsphere-measured perfusion data in vital organs.
microcirculation; extreme hemodilution; plasma expander; organ flow distribution; intravascular oxygen; functional capillary density
Address for reprint requests and other correspondence: P. Cabrales, La Jolla Bioengineering Institute, 505 Coast Blvd. South, La Jolla, CA 92037 (e-mail: pcabrales{at}ucsd.edu )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00394.2006</identifier><identifier>PMID: 16731641</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Anemia ; Anemia - blood ; Anemia - physiopathology ; Animals ; Blood Pressure - drug effects ; Blood Viscosity - drug effects ; Blood Viscosity - physiology ; Cardiovascular system ; Cricetinae ; Dextrans - pharmacology ; Erythrocyte Transfusion ; Hematocrit ; Hemodilution ; Hemoglobins - metabolism ; Male ; Mesocricetus ; Microcirculation - drug effects ; Microcirculation - physiology ; Microspheres ; Perfusion ; Plasma ; Plasma Substitutes - pharmacology ; Regional Blood Flow - drug effects ; Regional Blood Flow - physiology ; Stress, Mechanical ; Stress, Physiological - blood ; Studies ; Viscosity</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2006-11, Vol.291 (5), p.H2445-H2452</ispartof><rights>Copyright American Physiological Society Nov 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-5014152a61e62c155981d40806c5f416ebeda994984eec5339228acfeea164073</citedby><cites>FETCH-LOGICAL-c422t-5014152a61e62c155981d40806c5f416ebeda994984eec5339228acfeea164073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16731641$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cabrales, Pedro</creatorcontrib><creatorcontrib>Tsai, Amy G</creatorcontrib><title>Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1 La Jolla Bioengineering Institute; and 2 Department of Bioengineering, University of California, San Diego, La Jolla, California
Submitted 14 April 2006
; accepted in final form 24 May 2006
The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extreme hemodilution with low- and high-viscosity plasma expanders (LVPE and HVPE, respectively) to determine whether plasma viscosity is a factor in homeostasis during extreme anemic conditions. Moderated hemodilution was induced by two isovolemic steps performed with 6% 70-kDa dextran until systemic hematocrit (Hct) was reduced to 18% ( level 2 ). In a third isovolemic step, hemodilution with LVPE (6% 70-kDa dextran, 2.8 cP) or HVPE (6% 500-kDa dextran, 5.9 cP) reduced Hct to 11%. Systemic parameters, cardiac output (CO), organ flow distribution, microhemodynamics, and functional capillary density, were measured after each exchange dilution. Fluorescent-labeled microspheres were used to measure organ (brain, heart, kidney, liver, lung, and spleen) and window chamber blood flow. Final blood and plasma viscosities after the entire protocol were 2.1 and 1.4 cP, respectively, for LVPE and 2.8 and 2.2 cP, respectively, for HVPE (baseline = 4.2 and 1.2 cP, respectively). HVPE significantly elevated mean arterial pressure and CO compared with LVPE but did not increase vascular resistance. Functional capillary density was significantly higher for HVPE [87% (SD 7) of baseline] than for LVPE [42% (SD 11) of baseline]. Increases in mean arterial blood pressure, CO, and shear stress-mediated factors could be responsible for maintaining organ and microvascular perfusion after exchange with HVPE compared with LVPE. Microhemodynamic data corresponded to microsphere-measured perfusion data in vital organs.
microcirculation; extreme hemodilution; plasma expander; organ flow distribution; intravascular oxygen; functional capillary density
Address for reprint requests and other correspondence: P. Cabrales, La Jolla Bioengineering Institute, 505 Coast Blvd. South, La Jolla, CA 92037 (e-mail: pcabrales{at}ucsd.edu )</description><subject>Anemia</subject><subject>Anemia - blood</subject><subject>Anemia - physiopathology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Viscosity - drug effects</subject><subject>Blood Viscosity - physiology</subject><subject>Cardiovascular system</subject><subject>Cricetinae</subject><subject>Dextrans - pharmacology</subject><subject>Erythrocyte Transfusion</subject><subject>Hematocrit</subject><subject>Hemodilution</subject><subject>Hemoglobins - metabolism</subject><subject>Male</subject><subject>Mesocricetus</subject><subject>Microcirculation - drug effects</subject><subject>Microcirculation - physiology</subject><subject>Microspheres</subject><subject>Perfusion</subject><subject>Plasma</subject><subject>Plasma Substitutes - pharmacology</subject><subject>Regional Blood Flow - drug effects</subject><subject>Regional Blood Flow - physiology</subject><subject>Stress, Mechanical</subject><subject>Stress, Physiological - blood</subject><subject>Studies</subject><subject>Viscosity</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtrFEEUhQtRzBj9BYIULrLrSb27C1cSEiMEzCJZF5Xq2zM19Mt6RPvfW5MZjQiu7uKe73LPOQi9p2RNqWTndjdvwYa0JoRrsWaEqBdoVTasopLrl2hFuOKVolyeoDcx7gghslb8NTqhquZUCbpC3W1v42Dxo49uij4tOMAm9zZBxHGJCQbvsB1bXGaYHm10ZRnwDKHL0U8jbnPw4wZblxNg-JkCDFCAJ85NY-tTUcW36FVn-wjvjvMU3V9d3l1cVzffvny9-HxTOcFYqiShohiwioJijkqpG9oK0hDlZCeoggdordZCNwLASc41Y411HYAtdkjNT9HZ4e4cpu8ZYjJDMQZ9Xz6acjSq0bwWWhbhx3-EuymHsfxmGNOK1kKxIuIHUbEeY4DOzMEPNiyGErPvwPzuwDx1YPYdFOrD8XR-GKB9Zo6hF8H5QbD1m-0PH8DM26WE2U-b5fki09RIc82E2H_76f_EVe77u5L8H_Qv0sxtx38BseOsPQ</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Cabrales, Pedro</creator><creator>Tsai, Amy G</creator><general>American Physiological Society</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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20061101</creationdate><title>Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions</title><author>Cabrales, Pedro ; Tsai, Amy G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-5014152a61e62c155981d40806c5f416ebeda994984eec5339228acfeea164073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anemia</topic><topic>Anemia - blood</topic><topic>Anemia - physiopathology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Viscosity - drug effects</topic><topic>Blood Viscosity - physiology</topic><topic>Cardiovascular system</topic><topic>Cricetinae</topic><topic>Dextrans - pharmacology</topic><topic>Erythrocyte Transfusion</topic><topic>Hematocrit</topic><topic>Hemodilution</topic><topic>Hemoglobins - metabolism</topic><topic>Male</topic><topic>Mesocricetus</topic><topic>Microcirculation - drug effects</topic><topic>Microcirculation - physiology</topic><topic>Microspheres</topic><topic>Perfusion</topic><topic>Plasma</topic><topic>Plasma Substitutes - pharmacology</topic><topic>Regional Blood Flow - drug effects</topic><topic>Regional Blood Flow - physiology</topic><topic>Stress, Mechanical</topic><topic>Stress, Physiological - blood</topic><topic>Studies</topic><topic>Viscosity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cabrales, Pedro</creatorcontrib><creatorcontrib>Tsai, Amy G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cabrales, Pedro</au><au>Tsai, Amy G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>291</volume><issue>5</issue><spage>H2445</spage><epage>H2452</epage><pages>H2445-H2452</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>1 La Jolla Bioengineering Institute; and 2 Department of Bioengineering, University of California, San Diego, La Jolla, California
Submitted 14 April 2006
; accepted in final form 24 May 2006
The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extreme hemodilution with low- and high-viscosity plasma expanders (LVPE and HVPE, respectively) to determine whether plasma viscosity is a factor in homeostasis during extreme anemic conditions. Moderated hemodilution was induced by two isovolemic steps performed with 6% 70-kDa dextran until systemic hematocrit (Hct) was reduced to 18% ( level 2 ). In a third isovolemic step, hemodilution with LVPE (6% 70-kDa dextran, 2.8 cP) or HVPE (6% 500-kDa dextran, 5.9 cP) reduced Hct to 11%. Systemic parameters, cardiac output (CO), organ flow distribution, microhemodynamics, and functional capillary density, were measured after each exchange dilution. Fluorescent-labeled microspheres were used to measure organ (brain, heart, kidney, liver, lung, and spleen) and window chamber blood flow. Final blood and plasma viscosities after the entire protocol were 2.1 and 1.4 cP, respectively, for LVPE and 2.8 and 2.2 cP, respectively, for HVPE (baseline = 4.2 and 1.2 cP, respectively). HVPE significantly elevated mean arterial pressure and CO compared with LVPE but did not increase vascular resistance. Functional capillary density was significantly higher for HVPE [87% (SD 7) of baseline] than for LVPE [42% (SD 11) of baseline]. Increases in mean arterial blood pressure, CO, and shear stress-mediated factors could be responsible for maintaining organ and microvascular perfusion after exchange with HVPE compared with LVPE. Microhemodynamic data corresponded to microsphere-measured perfusion data in vital organs.
microcirculation; extreme hemodilution; plasma expander; organ flow distribution; intravascular oxygen; functional capillary density
Address for reprint requests and other correspondence: P. Cabrales, La Jolla Bioengineering Institute, 505 Coast Blvd. South, La Jolla, CA 92037 (e-mail: pcabrales{at}ucsd.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>16731641</pmid><doi>10.1152/ajpheart.00394.2006</doi></addata></record> |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Anemia Anemia - blood Anemia - physiopathology Animals Blood Pressure - drug effects Blood Viscosity - drug effects Blood Viscosity - physiology Cardiovascular system Cricetinae Dextrans - pharmacology Erythrocyte Transfusion Hematocrit Hemodilution Hemoglobins - metabolism Male Mesocricetus Microcirculation - drug effects Microcirculation - physiology Microspheres Perfusion Plasma Plasma Substitutes - pharmacology Regional Blood Flow - drug effects Regional Blood Flow - physiology Stress, Mechanical Stress, Physiological - blood Studies Viscosity |
title | Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions |
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