Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction
The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstri...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2004-10, Vol.56 (4), p.H1792-H1800 |
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container_title | American journal of physiology. Heart and circulatory physiology |
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creator | FRIESENECKER, B TSAI, A. G DÜNSER, M. W MAYR, A. J MARTINI, J KNOTZER, H HASIBEDER, W INTAGLIETTA, M |
description | The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU x kg-1 x min-1) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural PO2 difference. AVP caused tissue PO2 to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue PO2, and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue PO2. These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation. [PUBLICATION ABSTRACT] |
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G ; DÜNSER, M. W ; MAYR, A. J ; MARTINI, J ; KNOTZER, H ; HASIBEDER, W ; INTAGLIETTA, M</creator><creatorcontrib>FRIESENECKER, B ; TSAI, A. G ; DÜNSER, M. W ; MAYR, A. J ; MARTINI, J ; KNOTZER, H ; HASIBEDER, W ; INTAGLIETTA, M</creatorcontrib><description>The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU x kg-1 x min-1) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural PO2 difference. AVP caused tissue PO2 to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue PO2, and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue PO2. These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation. [PUBLICATION ABSTRACT]</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>Bethesda, MD: American Physiological Society</publisher><subject>Biological and medical sciences ; Circulatory system ; Coronary vessels ; Fundamental and applied biological sciences. Psychology ; Metabolism ; Oxygen ; Rodents ; Vertebrates: cardiovascular system</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2004-10, Vol.56 (4), p.H1792-H1800</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright American Physiological Society Oct 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16147608$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>FRIESENECKER, B</creatorcontrib><creatorcontrib>TSAI, A. G</creatorcontrib><creatorcontrib>DÜNSER, M. W</creatorcontrib><creatorcontrib>MAYR, A. J</creatorcontrib><creatorcontrib>MARTINI, J</creatorcontrib><creatorcontrib>KNOTZER, H</creatorcontrib><creatorcontrib>HASIBEDER, W</creatorcontrib><creatorcontrib>INTAGLIETTA, M</creatorcontrib><title>Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction</title><title>American journal of physiology. Heart and circulatory physiology</title><description>The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU x kg-1 x min-1) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural PO2 difference. AVP caused tissue PO2 to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue PO2, and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue PO2. These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation. [PUBLICATION ABSTRACT]</description><subject>Biological and medical sciences</subject><subject>Circulatory system</subject><subject>Coronary vessels</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Metabolism</subject><subject>Oxygen</subject><subject>Rodents</subject><subject>Vertebrates: cardiovascular system</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNotjctqwzAUREVpoW7afzCFLg2SZUnWsoS-IJBN9uZaj3CDI7mSXZq_r5NmNTBzZuaGFEzUdcUE17ekoFzySjIu7slDzgdKqVCSF8Rvf097F0qLeUrYzxPGUGIoj2hSNJjMPMDFAz-5VELaY8Dgyh_IcUwuZwwVBjsbZ5dwQTAOkC6xieG8ac71R3LnYcju6aorsnt_260_q83242v9uqlGoXQlQWrZ9Ap6S5WyYJWXupW81401igvBlW8ArGDC-1p7v6C6NVp5rWrRA1-R5__ZMcXv2eWpO8Q5heWxq2stWSuoXqCXKwTZwOATBIO5GxMeIZ06JlmjJG35HwhUY1E</recordid><startdate>20041001</startdate><enddate>20041001</enddate><creator>FRIESENECKER, B</creator><creator>TSAI, A. G</creator><creator>DÜNSER, M. W</creator><creator>MAYR, A. J</creator><creator>MARTINI, J</creator><creator>KNOTZER, H</creator><creator>HASIBEDER, W</creator><creator>INTAGLIETTA, M</creator><general>American Physiological Society</general><scope>IQODW</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></search><sort><creationdate>20041001</creationdate><title>Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction</title><author>FRIESENECKER, B ; TSAI, A. G ; DÜNSER, M. W ; MAYR, A. 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J</creatorcontrib><creatorcontrib>MARTINI, J</creatorcontrib><creatorcontrib>KNOTZER, H</creatorcontrib><creatorcontrib>HASIBEDER, W</creatorcontrib><creatorcontrib>INTAGLIETTA, M</creatorcontrib><collection>Pascal-Francis</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><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FRIESENECKER, B</au><au>TSAI, A. G</au><au>DÜNSER, M. W</au><au>MAYR, A. J</au><au>MARTINI, J</au><au>KNOTZER, H</au><au>HASIBEDER, W</au><au>INTAGLIETTA, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><date>2004-10-01</date><risdate>2004</risdate><volume>56</volume><issue>4</issue><spage>H1792</spage><epage>H1800</epage><pages>H1792-H1800</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU x kg-1 x min-1) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural PO2 difference. AVP caused tissue PO2 to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue PO2, and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue PO2. These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation. [PUBLICATION ABSTRACT]</abstract><cop>Bethesda, MD</cop><pub>American Physiological Society</pub></addata></record> |
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subjects | Biological and medical sciences Circulatory system Coronary vessels Fundamental and applied biological sciences. Psychology Metabolism Oxygen Rodents Vertebrates: cardiovascular system |
title | Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction |
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