Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia
1 Department of Physiology and Biomedical Engineering and the 2 Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota; and 3 Department of Biological Sciences, Minnesota State University, Mankato, Minnesota Submitted 11 August 2008 ; accepted in final form 24 October 2008 Ischem...
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creator | Warner, Lizette Gomez, Sabas I Bolterman, Rodney Haas, John A Bentley, Michael D Lerman, Lilach O Romero, Juan C |
description | 1 Department of Physiology and Biomedical Engineering and the 2 Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota; and 3 Department of Biological Sciences, Minnesota State University, Mankato, Minnesota
Submitted 11 August 2008
; accepted in final form 24 October 2008
Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O 2 delivery, and O 2 consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O 2 delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O 2 . Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O 2 consumption decreased proportionally to O 2 delivery during the graded stenosis (19 ± 10.8, 48.2 ± 9.1, 58.9 ± 4.7 vs. 15.1 ± 5, 35.4 ± 3.5, 57 ± 2.3%, respectively) while arterial venous O 2 differences were unchanged. Acute RAS produced a sharp reduction in O 2 efficiency for sodium reabsorption ( P < 0.01). Cortical decreases are exceeded by medullary decreases during stenosis (34.8 ± 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O 2 delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.
ischemia; renal tissue oxygenation; renal blood flow; pig
Address for reprint requests and other correspondence: J. C. Romero, Mayo Clinic, ST 7, 200 First St. SW, Rochester, MN, 55905 |
doi_str_mv | 10.1152/ajpregu.90677.2008 |
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Submitted 11 August 2008
; accepted in final form 24 October 2008
Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O 2 delivery, and O 2 consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O 2 delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O 2 . Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O 2 consumption decreased proportionally to O 2 delivery during the graded stenosis (19 ± 10.8, 48.2 ± 9.1, 58.9 ± 4.7 vs. 15.1 ± 5, 35.4 ± 3.5, 57 ± 2.3%, respectively) while arterial venous O 2 differences were unchanged. Acute RAS produced a sharp reduction in O 2 efficiency for sodium reabsorption ( P < 0.01). Cortical decreases are exceeded by medullary decreases during stenosis (34.8 ± 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O 2 delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.
ischemia; renal tissue oxygenation; renal blood flow; pig
Address for reprint requests and other correspondence: J. C. Romero, Mayo Clinic, ST 7, 200 First St. SW, Rochester, MN, 55905</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.90677.2008</identifier><identifier>PMID: 18971350</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Acute Disease ; Animals ; Disease Models, Animal ; Energy Metabolism ; Glomerular Filtration Rate ; Hemodynamics and Cardiorenal Integration ; Hypoxia - etiology ; Hypoxia - metabolism ; Hypoxia - physiopathology ; Ion-Selective Electrodes ; Ischemia - etiology ; Ischemia - metabolism ; Ischemia - physiopathology ; Kidney Cortex - blood supply ; Kidney Cortex - metabolism ; Kidney Medulla - blood supply ; Kidney Medulla - metabolism ; Oxygen - blood ; Oxygen - metabolism ; Oxygen Consumption ; Renal Artery Obstruction - complications ; Renal Artery Obstruction - metabolism ; Renal Artery Obstruction - physiopathology ; Renal Circulation ; Sodium - metabolism ; Sus scrofa</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2009-01, Vol.296 (1), p.R67-R71</ispartof><rights>Copyright © 2009, American Physiological Society 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-21f5ed42ab896e51abfb2464711f93b0217abd0e3ea9f8b318180322ccbaf5dd3</citedby><cites>FETCH-LOGICAL-c552t-21f5ed42ab896e51abfb2464711f93b0217abd0e3ea9f8b318180322ccbaf5dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18971350$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Warner, Lizette</creatorcontrib><creatorcontrib>Gomez, Sabas I</creatorcontrib><creatorcontrib>Bolterman, Rodney</creatorcontrib><creatorcontrib>Haas, John A</creatorcontrib><creatorcontrib>Bentley, Michael D</creatorcontrib><creatorcontrib>Lerman, Lilach O</creatorcontrib><creatorcontrib>Romero, Juan C</creatorcontrib><title>Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>1 Department of Physiology and Biomedical Engineering and the 2 Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota; and 3 Department of Biological Sciences, Minnesota State University, Mankato, Minnesota
Submitted 11 August 2008
; accepted in final form 24 October 2008
Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O 2 delivery, and O 2 consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O 2 delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O 2 . Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O 2 consumption decreased proportionally to O 2 delivery during the graded stenosis (19 ± 10.8, 48.2 ± 9.1, 58.9 ± 4.7 vs. 15.1 ± 5, 35.4 ± 3.5, 57 ± 2.3%, respectively) while arterial venous O 2 differences were unchanged. Acute RAS produced a sharp reduction in O 2 efficiency for sodium reabsorption ( P < 0.01). Cortical decreases are exceeded by medullary decreases during stenosis (34.8 ± 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O 2 delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.
ischemia; renal tissue oxygenation; renal blood flow; pig
Address for reprint requests and other correspondence: J. C. Romero, Mayo Clinic, ST 7, 200 First St. SW, Rochester, MN, 55905</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Energy Metabolism</subject><subject>Glomerular Filtration Rate</subject><subject>Hemodynamics and Cardiorenal Integration</subject><subject>Hypoxia - etiology</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - physiopathology</subject><subject>Ion-Selective Electrodes</subject><subject>Ischemia - etiology</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - physiopathology</subject><subject>Kidney Cortex - blood supply</subject><subject>Kidney Cortex - metabolism</subject><subject>Kidney Medulla - blood supply</subject><subject>Kidney Medulla - metabolism</subject><subject>Oxygen - blood</subject><subject>Oxygen - metabolism</subject><subject>Oxygen Consumption</subject><subject>Renal Artery Obstruction - complications</subject><subject>Renal Artery Obstruction - metabolism</subject><subject>Renal Artery Obstruction - physiopathology</subject><subject>Renal Circulation</subject><subject>Sodium - metabolism</subject><subject>Sus scrofa</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9v1DAQxS0EotvCF-CAfOJEFv9JnJgDEqpaQKqEVJWz5djjxFU2DnZSut8eLxsWOHDyyPN7b2b0EHpFyZbSir3T91OEbtlKIup6ywhpnqBNbrCClpI8RRvCBS8EpfIMnad0TwgpecmfozPayJryimzQeAudD6MesAUTQSdI2I84wuErPO67XMwZwHaJfuxwF7UFi7VZZlgpHWeIPhdphjEkn95jjU12wi7ElfHJ9LDz-gV65vSQ4OX6XqBv11d3l5-Lm6-fvlx-vClMVbG5YNRVYEum20YKqKhuXctKUdaUOslbwmitW0uAg5auaTltaEM4Y8a02lXW8gv04eg7Le0OrIFxjnpQU_Q7HfcqaK_-7Yy-V114UEyKkhOZDd6sBjF8XyDNapdvgGHQI4QlKSHqhsrqALIjaGJIKYI7DaFEHWJSa0zqV0zqEFMWvf57vT-SNZcMvD0Cve_6Hz6Cmvp98mEI3f5kmHdVVN2KOuPN__HrZRju4HH-rTvJ1GQd_wl1V7ib</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Warner, Lizette</creator><creator>Gomez, Sabas I</creator><creator>Bolterman, Rodney</creator><creator>Haas, John A</creator><creator>Bentley, Michael D</creator><creator>Lerman, Lilach O</creator><creator>Romero, Juan C</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090101</creationdate><title>Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia</title><author>Warner, Lizette ; Gomez, Sabas I ; Bolterman, Rodney ; Haas, John A ; Bentley, Michael D ; Lerman, Lilach O ; Romero, Juan C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-21f5ed42ab896e51abfb2464711f93b0217abd0e3ea9f8b318180322ccbaf5dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Energy Metabolism</topic><topic>Glomerular Filtration Rate</topic><topic>Hemodynamics and Cardiorenal Integration</topic><topic>Hypoxia - etiology</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - physiopathology</topic><topic>Ion-Selective Electrodes</topic><topic>Ischemia - etiology</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - physiopathology</topic><topic>Kidney Cortex - blood supply</topic><topic>Kidney Cortex - metabolism</topic><topic>Kidney Medulla - blood supply</topic><topic>Kidney Medulla - metabolism</topic><topic>Oxygen - blood</topic><topic>Oxygen - metabolism</topic><topic>Oxygen Consumption</topic><topic>Renal Artery Obstruction - complications</topic><topic>Renal Artery Obstruction - metabolism</topic><topic>Renal Artery Obstruction - physiopathology</topic><topic>Renal Circulation</topic><topic>Sodium - metabolism</topic><topic>Sus scrofa</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Warner, Lizette</creatorcontrib><creatorcontrib>Gomez, Sabas I</creatorcontrib><creatorcontrib>Bolterman, Rodney</creatorcontrib><creatorcontrib>Haas, John A</creatorcontrib><creatorcontrib>Bentley, Michael D</creatorcontrib><creatorcontrib>Lerman, Lilach O</creatorcontrib><creatorcontrib>Romero, Juan C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Warner, Lizette</au><au>Gomez, Sabas I</au><au>Bolterman, Rodney</au><au>Haas, John A</au><au>Bentley, Michael D</au><au>Lerman, Lilach O</au><au>Romero, Juan C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>296</volume><issue>1</issue><spage>R67</spage><epage>R71</epage><pages>R67-R71</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><abstract>1 Department of Physiology and Biomedical Engineering and the 2 Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota; and 3 Department of Biological Sciences, Minnesota State University, Mankato, Minnesota
Submitted 11 August 2008
; accepted in final form 24 October 2008
Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O 2 delivery, and O 2 consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O 2 delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O 2 . Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O 2 consumption decreased proportionally to O 2 delivery during the graded stenosis (19 ± 10.8, 48.2 ± 9.1, 58.9 ± 4.7 vs. 15.1 ± 5, 35.4 ± 3.5, 57 ± 2.3%, respectively) while arterial venous O 2 differences were unchanged. Acute RAS produced a sharp reduction in O 2 efficiency for sodium reabsorption ( P < 0.01). Cortical decreases are exceeded by medullary decreases during stenosis (34.8 ± 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O 2 delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.
ischemia; renal tissue oxygenation; renal blood flow; pig
Address for reprint requests and other correspondence: J. C. Romero, Mayo Clinic, ST 7, 200 First St. SW, Rochester, MN, 55905</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>18971350</pmid><doi>10.1152/ajpregu.90677.2008</doi><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Acute Disease Animals Disease Models, Animal Energy Metabolism Glomerular Filtration Rate Hemodynamics and Cardiorenal Integration Hypoxia - etiology Hypoxia - metabolism Hypoxia - physiopathology Ion-Selective Electrodes Ischemia - etiology Ischemia - metabolism Ischemia - physiopathology Kidney Cortex - blood supply Kidney Cortex - metabolism Kidney Medulla - blood supply Kidney Medulla - metabolism Oxygen - blood Oxygen - metabolism Oxygen Consumption Renal Artery Obstruction - complications Renal Artery Obstruction - metabolism Renal Artery Obstruction - physiopathology Renal Circulation Sodium - metabolism Sus scrofa |
title | Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia |
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