Electrophysiological Basis of Arteriolar Vasomotion in vivo
We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscill...
Gespeichert in:
| Veröffentlicht in: | Journal of vascular research 2000-11, Vol.37 (6), p.568-575 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 575 |
|---|---|
| container_issue | 6 |
| container_start_page | 568 |
| container_title | Journal of vascular research |
| container_volume | 37 |
| creator | Bartlett, Iain S. Crane, Glenis J. Neild, Timothy O. Segal, Steven S. |
| description | We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s –1 ) with no diameter change; (3) a fast (9.1 ± 0.8 mV s –1 ) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s –1 ) and relaxation. The absolute change in E m correlated (r = 0.60, p < 0.01) with the most negative E m . Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO 2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E m of SMC and EC corresponding with cation fluxes across plasma membranes. |
| doi_str_mv | 10.1159/000054090 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmed_primary_11146411</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67773479</sourcerecordid><originalsourceid>FETCH-LOGICAL-c449t-cf3bb8430a572dd5eb713de1e524ee878bdd78a6bd1d69a64601ba1949e054b63</originalsourceid><addsrcrecordid>eNpt0E1LxDAQBuAgiuvXwbMgZQXBQzXTJG2CJ5X1C0EQ9VrSJl2j3aYmrbD_3ujWFcRcEjIPM8mL0C7gYwAmTnBYjGKBV9AG0ITEGAhbDWcMPAbIkhHa9P4VY6CCp-toBAA0pQAb6HRS67Jztn2Ze2NrOzWlrKNz6Y2PbBWduU67cC9d9Cy9ndnO2CYyTfRhPuw2Wqtk7fXOsG-hp8vJ48V1fHd_dXNxdheXlIouLitSFJwSLFmWKMV0kQFRGjRLqNY844VSGZdpoUClQqY0xVBIEFTo8KsiJVvocNG3dfa9177LZ8aXuq5lo23v8yxhJBEUAhz_ga-2d014W54klDHMsQjoaIFKZ713uspbZ2bSzXPA-Vec-TLOYPeHhn0x0-pXDvkFcDAA6UNwlZNNafzS8ZRwmgW1t1Bv0k21W5Z_hoz_rd4-P3yDvFUV-QQgW48g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>224550809</pqid></control><display><type>article</type><title>Electrophysiological Basis of Arteriolar Vasomotion in vivo</title><source>Karger电子期刊和电子书数据库</source><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Bartlett, Iain S. ; Crane, Glenis J. ; Neild, Timothy O. ; Segal, Steven S.</creator><creatorcontrib>Bartlett, Iain S. ; Crane, Glenis J. ; Neild, Timothy O. ; Segal, Steven S.</creatorcontrib><description>We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s –1 ) with no diameter change; (3) a fast (9.1 ± 0.8 mV s –1 ) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s –1 ) and relaxation. The absolute change in E m correlated (r = 0.60, p < 0.01) with the most negative E m . Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO 2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E m of SMC and EC corresponding with cation fluxes across plasma membranes.</description><identifier>ISSN: 1018-1172</identifier><identifier>EISSN: 1423-0135</identifier><identifier>DOI: 10.1159/000054090</identifier><identifier>PMID: 11146411</identifier><identifier>CODEN: JVREE9</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Action Potentials - drug effects ; Animals ; Arterioles - physiology ; Biological and medical sciences ; Calcium - metabolism ; Calcium Channel Blockers - pharmacology ; Calcium Channels, L-Type - drug effects ; Cricetinae ; Electrophysiology ; Fundamental and applied biological sciences. Psychology ; Indoles - pharmacology ; Ion Transport - drug effects ; Male ; Membrane Potentials - drug effects ; Mesocricetus ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Nifedipine - pharmacology ; Nitroprusside - pharmacology ; Oxygen - physiology ; Partial Pressure ; Potassium Channel Blockers ; Research Paper ; Striated muscle. Tendons ; Tetraethylammonium - pharmacology ; Vasoconstriction - physiology ; Vasodilator Agents - pharmacology ; Vasomotor System - drug effects ; Vasomotor System - physiology ; Vertebrates: osteoarticular system, musculoskeletal system</subject><ispartof>Journal of vascular research, 2000-11, Vol.37 (6), p.568-575</ispartof><rights>2000 S. Karger AG, Basel</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2000 S. Karger AG, Basel</rights><rights>Copyright S. Karger AG Nov/Dec 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-cf3bb8430a572dd5eb713de1e524ee878bdd78a6bd1d69a64601ba1949e054b63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,777,781,786,787,2423,23911,23912,25121,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=863847$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11146411$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bartlett, Iain S.</creatorcontrib><creatorcontrib>Crane, Glenis J.</creatorcontrib><creatorcontrib>Neild, Timothy O.</creatorcontrib><creatorcontrib>Segal, Steven S.</creatorcontrib><title>Electrophysiological Basis of Arteriolar Vasomotion in vivo</title><title>Journal of vascular research</title><addtitle>J Vasc Res</addtitle><description>We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s –1 ) with no diameter change; (3) a fast (9.1 ± 0.8 mV s –1 ) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s –1 ) and relaxation. The absolute change in E m correlated (r = 0.60, p < 0.01) with the most negative E m . Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO 2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E m of SMC and EC corresponding with cation fluxes across plasma membranes.</description><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Arterioles - physiology</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Channels, L-Type - drug effects</subject><subject>Cricetinae</subject><subject>Electrophysiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Indoles - pharmacology</subject><subject>Ion Transport - drug effects</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>Mesocricetus</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Nifedipine - pharmacology</subject><subject>Nitroprusside - pharmacology</subject><subject>Oxygen - physiology</subject><subject>Partial Pressure</subject><subject>Potassium Channel Blockers</subject><subject>Research Paper</subject><subject>Striated muscle. Tendons</subject><subject>Tetraethylammonium - pharmacology</subject><subject>Vasoconstriction - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasomotor System - drug effects</subject><subject>Vasomotor System - physiology</subject><subject>Vertebrates: osteoarticular system, musculoskeletal system</subject><issn>1018-1172</issn><issn>1423-0135</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</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><sourceid>GNUQQ</sourceid><recordid>eNpt0E1LxDAQBuAgiuvXwbMgZQXBQzXTJG2CJ5X1C0EQ9VrSJl2j3aYmrbD_3ujWFcRcEjIPM8mL0C7gYwAmTnBYjGKBV9AG0ITEGAhbDWcMPAbIkhHa9P4VY6CCp-toBAA0pQAb6HRS67Jztn2Ze2NrOzWlrKNz6Y2PbBWduU67cC9d9Cy9ndnO2CYyTfRhPuw2Wqtk7fXOsG-hp8vJ48V1fHd_dXNxdheXlIouLitSFJwSLFmWKMV0kQFRGjRLqNY844VSGZdpoUClQqY0xVBIEFTo8KsiJVvocNG3dfa9177LZ8aXuq5lo23v8yxhJBEUAhz_ga-2d014W54klDHMsQjoaIFKZ713uspbZ2bSzXPA-Vec-TLOYPeHhn0x0-pXDvkFcDAA6UNwlZNNafzS8ZRwmgW1t1Bv0k21W5Z_hoz_rd4-P3yDvFUV-QQgW48g</recordid><startdate>20001101</startdate><enddate>20001101</enddate><creator>Bartlett, Iain S.</creator><creator>Crane, Glenis J.</creator><creator>Neild, Timothy O.</creator><creator>Segal, Steven S.</creator><general>Karger</general><general>S. Karger AG</general><scope>IQODW</scope><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>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20001101</creationdate><title>Electrophysiological Basis of Arteriolar Vasomotion in vivo</title><author>Bartlett, Iain S. ; Crane, Glenis J. ; Neild, Timothy O. ; Segal, Steven S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-cf3bb8430a572dd5eb713de1e524ee878bdd78a6bd1d69a64601ba1949e054b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Arterioles - physiology</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Channels, L-Type - drug effects</topic><topic>Cricetinae</topic><topic>Electrophysiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Indoles - pharmacology</topic><topic>Ion Transport - drug effects</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>Mesocricetus</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Nifedipine - pharmacology</topic><topic>Nitroprusside - pharmacology</topic><topic>Oxygen - physiology</topic><topic>Partial Pressure</topic><topic>Potassium Channel Blockers</topic><topic>Research Paper</topic><topic>Striated muscle. Tendons</topic><topic>Tetraethylammonium - pharmacology</topic><topic>Vasoconstriction - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasomotor System - drug effects</topic><topic>Vasomotor System - physiology</topic><topic>Vertebrates: osteoarticular system, musculoskeletal system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bartlett, Iain S.</creatorcontrib><creatorcontrib>Crane, Glenis J.</creatorcontrib><creatorcontrib>Neild, Timothy O.</creatorcontrib><creatorcontrib>Segal, Steven S.</creatorcontrib><collection>Pascal-Francis</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Science Journals</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of vascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bartlett, Iain S.</au><au>Crane, Glenis J.</au><au>Neild, Timothy O.</au><au>Segal, Steven S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electrophysiological Basis of Arteriolar Vasomotion in vivo</atitle><jtitle>Journal of vascular research</jtitle><addtitle>J Vasc Res</addtitle><date>2000-11-01</date><risdate>2000</risdate><volume>37</volume><issue>6</issue><spage>568</spage><epage>575</epage><pages>568-575</pages><issn>1018-1172</issn><eissn>1423-0135</eissn><coden>JVREE9</coden><abstract>We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s –1 ) with no diameter change; (3) a fast (9.1 ± 0.8 mV s –1 ) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s –1 ) and relaxation. The absolute change in E m correlated (r = 0.60, p < 0.01) with the most negative E m . Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO 2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E m of SMC and EC corresponding with cation fluxes across plasma membranes.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>11146411</pmid><doi>10.1159/000054090</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1018-1172 |
| ispartof | Journal of vascular research, 2000-11, Vol.37 (6), p.568-575 |
| issn | 1018-1172 1423-0135 |
| language | eng |
| recordid | cdi_pubmed_primary_11146411 |
| source | Karger电子期刊和电子书数据库; MEDLINE; Alma/SFX Local Collection |
| subjects | Action Potentials - drug effects Animals Arterioles - physiology Biological and medical sciences Calcium - metabolism Calcium Channel Blockers - pharmacology Calcium Channels, L-Type - drug effects Cricetinae Electrophysiology Fundamental and applied biological sciences. Psychology Indoles - pharmacology Ion Transport - drug effects Male Membrane Potentials - drug effects Mesocricetus Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Nifedipine - pharmacology Nitroprusside - pharmacology Oxygen - physiology Partial Pressure Potassium Channel Blockers Research Paper Striated muscle. Tendons Tetraethylammonium - pharmacology Vasoconstriction - physiology Vasodilator Agents - pharmacology Vasomotor System - drug effects Vasomotor System - physiology Vertebrates: osteoarticular system, musculoskeletal system |
| title | Electrophysiological Basis of Arteriolar Vasomotion in vivo |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T17%3A20%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Electrophysiological%20Basis%20of%20Arteriolar%20Vasomotion%20in%20vivo&rft.jtitle=Journal%20of%20vascular%20research&rft.au=Bartlett,%20Iain%20S.&rft.date=2000-11-01&rft.volume=37&rft.issue=6&rft.spage=568&rft.epage=575&rft.pages=568-575&rft.issn=1018-1172&rft.eissn=1423-0135&rft.coden=JVREE9&rft_id=info:doi/10.1159/000054090&rft_dat=%3Cproquest_pubme%3E67773479%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=224550809&rft_id=info:pmid/11146411&rfr_iscdi=true |