Postconditioning in major vascular surgery: prevention of renal failure
Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure. Bilateral lower limb ischemia was induced in male W...
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creator | Aranyi, Peter Turoczi, Zsolt Garbaisz, David Lotz, Gabor Geleji, Janos Hegedus, Viktor Rakonczay, Zoltan Balla, Zsolt Harsanyi, Laszlo Szijarto, Attila |
description | Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure.
Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter.
Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs. PostC: 0.92 ± 0.32 mM; 24 h: IR: 1.53 ± 0.45 mM vs. PostC: 0.77 ± 0.34 mM; 72 h: IR: 1.51 ± 0.36 mM vs. PostC: 0.43 ± 0.28 mM), while systemic hemodynamics and kidney microcirculation significantly improved (calculated reperfusion area: IR: 82.31 ± 12.23% vs. PostC: 99.01 ± 2.76%), and arterial blood gas analysis showed a lesser extent systemic acidic load after revascularization (a defined relative base excess parameter: 1(st) s: IR: 2.25 ± 1.14 vs. PostC: 1.80 ± 0.66; 2(nd) s: IR: 2.14 ± 1.44 vs. PostC: 2.44 ± 1.14, 3(rd) s: IR: 3.99 ± 3.09 vs. PostC: 2.07 ± 0.82; 4(th) s: IR: 3.28 ± 0.32 vs. PostC: 2.05 ± 0.56).
The results suggest a protective role for postconditioning in major vascular surgeries against renal complications through a possible alternative release of nephrotoxic agents and exerting a positive effect on hemodynamic stability. |
doi_str_mv | 10.1186/s12967-014-0379-7 |
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fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4314807</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A542050683</galeid><sourcerecordid>A542050683</sourcerecordid><originalsourceid>FETCH-LOGICAL-c466t-423f400f8d54761140a4354f0e1d66787dd36aa069d240977aacdc1625bab16b3</originalsourceid><addsrcrecordid>eNptkc9LwzAcxYMobk7_AC8S8NyZtGnSehDG0CkM9KDnkObHzGibkayD_femVMcGkkO-JO89XvIB4BajKcYFfQg4LSlLECYJyliZsDMwxiQOecHo-dE8AlchrBFKSU7KSzBKc5r21jFYfLiwla5Vdmtda9sVtC1sxNp5uBNBdrXwMHR-pf3-EW683um2F0JnoNetqKERtu68vgYXRtRB3_zuE_D18vw5f02W74u3-WyZSELpNiFpZghCplA5YRRjggTJcmKQxopSVjClMioEoqVKCSoZE0IqiWmaV6LCtMom4GnI3XRVo5WMdbyo-cbbRvg9d8Ly05vWfvOV23GSYVIgFgPuh4CVqDW3rXFRJhsbJJ_lJEU5okUWVdN_VHEp3dj4XdrYeH5iwINBeheC1-ZQCSPew-IDLB5h8R4W76vcHb_l4Pijk_0A8FuQAQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Postconditioning in major vascular surgery: prevention of renal failure</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>SpringerLink Journals - AutoHoldings</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><creator>Aranyi, Peter ; Turoczi, Zsolt ; Garbaisz, David ; Lotz, Gabor ; Geleji, Janos ; Hegedus, Viktor ; Rakonczay, Zoltan ; Balla, Zsolt ; Harsanyi, Laszlo ; Szijarto, Attila</creator><creatorcontrib>Aranyi, Peter ; Turoczi, Zsolt ; Garbaisz, David ; Lotz, Gabor ; Geleji, Janos ; Hegedus, Viktor ; Rakonczay, Zoltan ; Balla, Zsolt ; Harsanyi, Laszlo ; Szijarto, Attila</creatorcontrib><description>Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure.
Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter.
Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs. PostC: 0.92 ± 0.32 mM; 24 h: IR: 1.53 ± 0.45 mM vs. PostC: 0.77 ± 0.34 mM; 72 h: IR: 1.51 ± 0.36 mM vs. PostC: 0.43 ± 0.28 mM), while systemic hemodynamics and kidney microcirculation significantly improved (calculated reperfusion area: IR: 82.31 ± 12.23% vs. PostC: 99.01 ± 2.76%), and arterial blood gas analysis showed a lesser extent systemic acidic load after revascularization (a defined relative base excess parameter: 1(st) s: IR: 2.25 ± 1.14 vs. PostC: 1.80 ± 0.66; 2(nd) s: IR: 2.14 ± 1.44 vs. PostC: 2.44 ± 1.14, 3(rd) s: IR: 3.99 ± 3.09 vs. PostC: 2.07 ± 0.82; 4(th) s: IR: 3.28 ± 0.32 vs. PostC: 2.05 ± 0.56).
The results suggest a protective role for postconditioning in major vascular surgeries against renal complications through a possible alternative release of nephrotoxic agents and exerting a positive effect on hemodynamic stability.</description><identifier>ISSN: 1479-5876</identifier><identifier>EISSN: 1479-5876</identifier><identifier>DOI: 10.1186/s12967-014-0379-7</identifier><identifier>PMID: 25622967</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Blood gases ; Care and treatment ; Health aspects ; Hemodynamics ; HSP72 Heat-Shock Proteins - metabolism ; Immunohistochemistry ; Ischemia ; Ischemic Postconditioning ; Kidney Cortex - blood supply ; Kidney Cortex - pathology ; Kidney Cortex - physiopathology ; Kidney failure ; Kidney Function Tests ; Laser-Doppler Flowmetry ; Lipid Peroxidation ; Lower Extremity - blood supply ; Lower Extremity - physiopathology ; Male ; Microcirculation ; Muscles - pathology ; Myoglobin ; Myoglobin - metabolism ; Rats, Wistar ; Renal Insufficiency - etiology ; Renal Insufficiency - physiopathology ; Renal Insufficiency - prevention & control ; Reperfusion Injury - prevention & control ; Vascular Surgical Procedures - adverse effects</subject><ispartof>Journal of translational medicine, 2015-01, Vol.13 (1), p.21, Article 21</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Aranyi et al.; licensee BioMed Central. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-423f400f8d54761140a4354f0e1d66787dd36aa069d240977aacdc1625bab16b3</citedby><cites>FETCH-LOGICAL-c466t-423f400f8d54761140a4354f0e1d66787dd36aa069d240977aacdc1625bab16b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314807/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314807/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25622967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aranyi, Peter</creatorcontrib><creatorcontrib>Turoczi, Zsolt</creatorcontrib><creatorcontrib>Garbaisz, David</creatorcontrib><creatorcontrib>Lotz, Gabor</creatorcontrib><creatorcontrib>Geleji, Janos</creatorcontrib><creatorcontrib>Hegedus, Viktor</creatorcontrib><creatorcontrib>Rakonczay, Zoltan</creatorcontrib><creatorcontrib>Balla, Zsolt</creatorcontrib><creatorcontrib>Harsanyi, Laszlo</creatorcontrib><creatorcontrib>Szijarto, Attila</creatorcontrib><title>Postconditioning in major vascular surgery: prevention of renal failure</title><title>Journal of translational medicine</title><addtitle>J Transl Med</addtitle><description>Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure.
Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter.
Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs. PostC: 0.92 ± 0.32 mM; 24 h: IR: 1.53 ± 0.45 mM vs. PostC: 0.77 ± 0.34 mM; 72 h: IR: 1.51 ± 0.36 mM vs. PostC: 0.43 ± 0.28 mM), while systemic hemodynamics and kidney microcirculation significantly improved (calculated reperfusion area: IR: 82.31 ± 12.23% vs. PostC: 99.01 ± 2.76%), and arterial blood gas analysis showed a lesser extent systemic acidic load after revascularization (a defined relative base excess parameter: 1(st) s: IR: 2.25 ± 1.14 vs. PostC: 1.80 ± 0.66; 2(nd) s: IR: 2.14 ± 1.44 vs. PostC: 2.44 ± 1.14, 3(rd) s: IR: 3.99 ± 3.09 vs. PostC: 2.07 ± 0.82; 4(th) s: IR: 3.28 ± 0.32 vs. PostC: 2.05 ± 0.56).
The results suggest a protective role for postconditioning in major vascular surgeries against renal complications through a possible alternative release of nephrotoxic agents and exerting a positive effect on hemodynamic stability.</description><subject>Analysis</subject><subject>Animals</subject><subject>Blood gases</subject><subject>Care and treatment</subject><subject>Health aspects</subject><subject>Hemodynamics</subject><subject>HSP72 Heat-Shock Proteins - metabolism</subject><subject>Immunohistochemistry</subject><subject>Ischemia</subject><subject>Ischemic Postconditioning</subject><subject>Kidney Cortex - blood supply</subject><subject>Kidney Cortex - pathology</subject><subject>Kidney Cortex - physiopathology</subject><subject>Kidney failure</subject><subject>Kidney Function Tests</subject><subject>Laser-Doppler Flowmetry</subject><subject>Lipid Peroxidation</subject><subject>Lower Extremity - blood supply</subject><subject>Lower Extremity - physiopathology</subject><subject>Male</subject><subject>Microcirculation</subject><subject>Muscles - pathology</subject><subject>Myoglobin</subject><subject>Myoglobin - metabolism</subject><subject>Rats, Wistar</subject><subject>Renal Insufficiency - etiology</subject><subject>Renal Insufficiency - physiopathology</subject><subject>Renal Insufficiency - prevention & control</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Vascular Surgical Procedures - adverse effects</subject><issn>1479-5876</issn><issn>1479-5876</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkc9LwzAcxYMobk7_AC8S8NyZtGnSehDG0CkM9KDnkObHzGibkayD_femVMcGkkO-JO89XvIB4BajKcYFfQg4LSlLECYJyliZsDMwxiQOecHo-dE8AlchrBFKSU7KSzBKc5r21jFYfLiwla5Vdmtda9sVtC1sxNp5uBNBdrXwMHR-pf3-EW683um2F0JnoNetqKERtu68vgYXRtRB3_zuE_D18vw5f02W74u3-WyZSELpNiFpZghCplA5YRRjggTJcmKQxopSVjClMioEoqVKCSoZE0IqiWmaV6LCtMom4GnI3XRVo5WMdbyo-cbbRvg9d8Ly05vWfvOV23GSYVIgFgPuh4CVqDW3rXFRJhsbJJ_lJEU5okUWVdN_VHEp3dj4XdrYeH5iwINBeheC1-ZQCSPew-IDLB5h8R4W76vcHb_l4Pijk_0A8FuQAQ</recordid><startdate>20150127</startdate><enddate>20150127</enddate><creator>Aranyi, Peter</creator><creator>Turoczi, Zsolt</creator><creator>Garbaisz, David</creator><creator>Lotz, Gabor</creator><creator>Geleji, Janos</creator><creator>Hegedus, Viktor</creator><creator>Rakonczay, Zoltan</creator><creator>Balla, Zsolt</creator><creator>Harsanyi, Laszlo</creator><creator>Szijarto, Attila</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>5PM</scope></search><sort><creationdate>20150127</creationdate><title>Postconditioning in major vascular surgery: prevention of renal failure</title><author>Aranyi, Peter ; Turoczi, Zsolt ; Garbaisz, David ; Lotz, Gabor ; Geleji, Janos ; Hegedus, Viktor ; Rakonczay, Zoltan ; Balla, Zsolt ; Harsanyi, Laszlo ; Szijarto, Attila</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-423f400f8d54761140a4354f0e1d66787dd36aa069d240977aacdc1625bab16b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Blood gases</topic><topic>Care and treatment</topic><topic>Health aspects</topic><topic>Hemodynamics</topic><topic>HSP72 Heat-Shock Proteins - metabolism</topic><topic>Immunohistochemistry</topic><topic>Ischemia</topic><topic>Ischemic Postconditioning</topic><topic>Kidney Cortex - blood supply</topic><topic>Kidney Cortex - pathology</topic><topic>Kidney Cortex - physiopathology</topic><topic>Kidney failure</topic><topic>Kidney Function Tests</topic><topic>Laser-Doppler Flowmetry</topic><topic>Lipid Peroxidation</topic><topic>Lower Extremity - blood supply</topic><topic>Lower Extremity - physiopathology</topic><topic>Male</topic><topic>Microcirculation</topic><topic>Muscles - pathology</topic><topic>Myoglobin</topic><topic>Myoglobin - metabolism</topic><topic>Rats, Wistar</topic><topic>Renal Insufficiency - etiology</topic><topic>Renal Insufficiency - physiopathology</topic><topic>Renal Insufficiency - prevention & control</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Vascular Surgical Procedures - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aranyi, Peter</creatorcontrib><creatorcontrib>Turoczi, Zsolt</creatorcontrib><creatorcontrib>Garbaisz, David</creatorcontrib><creatorcontrib>Lotz, Gabor</creatorcontrib><creatorcontrib>Geleji, Janos</creatorcontrib><creatorcontrib>Hegedus, Viktor</creatorcontrib><creatorcontrib>Rakonczay, Zoltan</creatorcontrib><creatorcontrib>Balla, Zsolt</creatorcontrib><creatorcontrib>Harsanyi, Laszlo</creatorcontrib><creatorcontrib>Szijarto, Attila</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of translational medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aranyi, Peter</au><au>Turoczi, Zsolt</au><au>Garbaisz, David</au><au>Lotz, Gabor</au><au>Geleji, Janos</au><au>Hegedus, Viktor</au><au>Rakonczay, Zoltan</au><au>Balla, Zsolt</au><au>Harsanyi, Laszlo</au><au>Szijarto, Attila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Postconditioning in major vascular surgery: prevention of renal failure</atitle><jtitle>Journal of translational medicine</jtitle><addtitle>J Transl Med</addtitle><date>2015-01-27</date><risdate>2015</risdate><volume>13</volume><issue>1</issue><spage>21</spage><pages>21-</pages><artnum>21</artnum><issn>1479-5876</issn><eissn>1479-5876</eissn><abstract>Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure.
Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter.
Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs. PostC: 0.92 ± 0.32 mM; 24 h: IR: 1.53 ± 0.45 mM vs. PostC: 0.77 ± 0.34 mM; 72 h: IR: 1.51 ± 0.36 mM vs. PostC: 0.43 ± 0.28 mM), while systemic hemodynamics and kidney microcirculation significantly improved (calculated reperfusion area: IR: 82.31 ± 12.23% vs. PostC: 99.01 ± 2.76%), and arterial blood gas analysis showed a lesser extent systemic acidic load after revascularization (a defined relative base excess parameter: 1(st) s: IR: 2.25 ± 1.14 vs. PostC: 1.80 ± 0.66; 2(nd) s: IR: 2.14 ± 1.44 vs. PostC: 2.44 ± 1.14, 3(rd) s: IR: 3.99 ± 3.09 vs. PostC: 2.07 ± 0.82; 4(th) s: IR: 3.28 ± 0.32 vs. PostC: 2.05 ± 0.56).
The results suggest a protective role for postconditioning in major vascular surgeries against renal complications through a possible alternative release of nephrotoxic agents and exerting a positive effect on hemodynamic stability.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25622967</pmid><doi>10.1186/s12967-014-0379-7</doi><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Animals Blood gases Care and treatment Health aspects Hemodynamics HSP72 Heat-Shock Proteins - metabolism Immunohistochemistry Ischemia Ischemic Postconditioning Kidney Cortex - blood supply Kidney Cortex - pathology Kidney Cortex - physiopathology Kidney failure Kidney Function Tests Laser-Doppler Flowmetry Lipid Peroxidation Lower Extremity - blood supply Lower Extremity - physiopathology Male Microcirculation Muscles - pathology Myoglobin Myoglobin - metabolism Rats, Wistar Renal Insufficiency - etiology Renal Insufficiency - physiopathology Renal Insufficiency - prevention & control Reperfusion Injury - prevention & control Vascular Surgical Procedures - adverse effects |
title | Postconditioning in major vascular surgery: prevention of renal failure |
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