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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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2009-01, Vol.296 (1), p.R67-R71
Hauptverfasser: Warner, Lizette, Gomez, Sabas I, Bolterman, Rodney, Haas, John A, Bentley, Michael D, Lerman, Lilach O, Romero, Juan C
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container_end_page R71
container_issue 1
container_start_page R67
container_title American journal of physiology. Regulatory, integrative and comparative physiology
container_volume 296
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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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 &lt; 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. 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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 &lt; 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. 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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 &lt; 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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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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