Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation
Background The start of warm ischemic time (WIT) of donor lungs in donation after cardiac death (DCD) is not clearly defined. We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplant...
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Veröffentlicht in: | The Journal of heart and lung transplantation 2011-04, Vol.30 (4), p.445-451 |
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creator | Miyoshi, Kentaroh, MD Oto, Takahiro, MD Otani, Shinji, MD Tanaka, Shin, MD Harada, Masaaki, MD Kakishita, Tomokazu, MD Hori, Shiro, MD Waki, Naohisa, MD Yamane, Masaomi, MD Miyoshi, Shinichiro, MD |
description | Background The start of warm ischemic time (WIT) of donor lungs in donation after cardiac death (DCD) is not clearly defined. We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplantation. Methods Twenty mechanically-ventilated donor pigs were placed in 4 groups ( n = 5 each) and exposed to each of the pseudo-agonal conditions for 60 minutes: (1) control group, no intervention and optimum ventilation, followed by cardiac arrest; (2) hypotension (HT) group, controlled cardiac tamponade reducing systolic blood pressure to |
doi_str_mv | 10.1016/j.healun.2010.11.010 |
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We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplantation. Methods Twenty mechanically-ventilated donor pigs were placed in 4 groups ( n = 5 each) and exposed to each of the pseudo-agonal conditions for 60 minutes: (1) control group, no intervention and optimum ventilation, followed by cardiac arrest; (2) hypotension (HT) group, controlled cardiac tamponade reducing systolic blood pressure to <50 mm Hg, followed by cardiac arrest; (3) hypoventilation (HV) group, ventilation with room air at 5 breaths/min, followed by cardiac arrest; (4) non-circulation (NC) group, initial cardiac arrest, followed by a 60-minute standoff time. The lung graft was retrieved and the left lung was transplanted to the recipient. Graft function was evaluated for 4 hours after contralateral pulmonary artery ligation. The reperfusion injury was evaluated based on tissue cytokine expression, wet weight-to-dry weight ratio, and histology at the end of the reperfusion period. Results Impaired post-transplant graft function was seen in the HV group, which had significantly poorer oxygenation during the reperfusion period than the other groups ( p < 0.001). The HV group also had higher tissue levels of interleukin-8 ( p < 0.05), a higher wet weight-to-dry weight ratio ( p < 0.05), and histologic findings of graft tissue injury than the control group. The difference in these parameters among the control, HT, and NC groups was not significant. Conclusions Only pre-mortem hypoxia provoked by hypoventilation significantly impaired lung graft function in DCD lung transplantation. Ventilatory rather than circulatory deterioration can trigger the onset of warm ischemia.</description><identifier>ISSN: 1053-2498</identifier><identifier>EISSN: 1557-3117</identifier><identifier>DOI: 10.1016/j.healun.2010.11.010</identifier><identifier>PMID: 21211993</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Death ; definition ; donation after cardiac death (DCD) ; hypotension ; Hypotension - complications ; hypoxia ; Hypoxia - complications ; Lung - physiopathology ; Lung Transplantation ; Medical sciences ; Surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Swine ; Warm Ischemia ; warm ischemic time (WIT)</subject><ispartof>The Journal of heart and lung transplantation, 2011-04, Vol.30 (4), p.445-451</ispartof><rights>International Society for Heart and Lung Transplantation</rights><rights>2011 International Society for Heart and Lung Transplantation</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-47f9f69184537bf7d62454fda9f9b2403978ca72a0f2db88022f0c3678a69ae43</citedby><cites>FETCH-LOGICAL-c558t-47f9f69184537bf7d62454fda9f9b2403978ca72a0f2db88022f0c3678a69ae43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S105324981000762X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24043323$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21211993$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miyoshi, Kentaroh, MD</creatorcontrib><creatorcontrib>Oto, Takahiro, MD</creatorcontrib><creatorcontrib>Otani, Shinji, MD</creatorcontrib><creatorcontrib>Tanaka, Shin, MD</creatorcontrib><creatorcontrib>Harada, Masaaki, MD</creatorcontrib><creatorcontrib>Kakishita, Tomokazu, MD</creatorcontrib><creatorcontrib>Hori, Shiro, MD</creatorcontrib><creatorcontrib>Waki, Naohisa, MD</creatorcontrib><creatorcontrib>Yamane, Masaomi, MD</creatorcontrib><creatorcontrib>Miyoshi, Shinichiro, MD</creatorcontrib><title>Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation</title><title>The Journal of heart and lung transplantation</title><addtitle>J Heart Lung Transplant</addtitle><description>Background The start of warm ischemic time (WIT) of donor lungs in donation after cardiac death (DCD) is not clearly defined. We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplantation. Methods Twenty mechanically-ventilated donor pigs were placed in 4 groups ( n = 5 each) and exposed to each of the pseudo-agonal conditions for 60 minutes: (1) control group, no intervention and optimum ventilation, followed by cardiac arrest; (2) hypotension (HT) group, controlled cardiac tamponade reducing systolic blood pressure to <50 mm Hg, followed by cardiac arrest; (3) hypoventilation (HV) group, ventilation with room air at 5 breaths/min, followed by cardiac arrest; (4) non-circulation (NC) group, initial cardiac arrest, followed by a 60-minute standoff time. The lung graft was retrieved and the left lung was transplanted to the recipient. Graft function was evaluated for 4 hours after contralateral pulmonary artery ligation. The reperfusion injury was evaluated based on tissue cytokine expression, wet weight-to-dry weight ratio, and histology at the end of the reperfusion period. Results Impaired post-transplant graft function was seen in the HV group, which had significantly poorer oxygenation during the reperfusion period than the other groups ( p < 0.001). The HV group also had higher tissue levels of interleukin-8 ( p < 0.05), a higher wet weight-to-dry weight ratio ( p < 0.05), and histologic findings of graft tissue injury than the control group. The difference in these parameters among the control, HT, and NC groups was not significant. Conclusions Only pre-mortem hypoxia provoked by hypoventilation significantly impaired lung graft function in DCD lung transplantation. Ventilatory rather than circulatory deterioration can trigger the onset of warm ischemia.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Death</subject><subject>definition</subject><subject>donation after cardiac death (DCD)</subject><subject>hypotension</subject><subject>Hypotension - complications</subject><subject>hypoxia</subject><subject>Hypoxia - complications</subject><subject>Lung - physiopathology</subject><subject>Lung Transplantation</subject><subject>Medical sciences</subject><subject>Surgery</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>Swine</subject><subject>Warm Ischemia</subject><subject>warm ischemic time (WIT)</subject><issn>1053-2498</issn><issn>1557-3117</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks2KFDEQxxtR3HX1DURyEU895qs76Ysgy64KCx5U8BZq0slOxu6kTdLrznv4wKanRwUvQqCK4lcfqX9V1XOCNwST9vV-szMwzH5D8RIim2IeVOekaUTNCBEPi48bVlPeybPqSUp7jDFlDX1cnVFCCek6dl79vLLW6IyCRX3wIaIpmnoMMZsR7Q5TuHeAwPdHPxufXPCovNsINiM7e52XyEKkDPFY5wfEEbmkd2Ysyc4vhWHFbDYRaYi9A416A3mHyg9uUY7g0zSAz0fwafXIwpDMs5O9qL5cX32-fF_ffHz34fLtTa2bRuaaC9vZtiOSN0xsrehbyhtue-hst6Ucs05IDYICtrTfSokptVizVkhoOzCcXVSv1rpTDN9nk7Iay9xmKIOYMCclG0klF1IUkq-kjiGlaKyaohshHhTBapFD7dUqh1rkUISoYkrai1ODeTua_k_S7_0X4OUJgKRhsGUP2qW_HMecMbpwb1bOlHXcORNV0s54bXoXi3yqD-5_k_xbQA_Ou9LzmzmYtA9z9GXViqhEFVafltNZLoeUoxEt_cp-Aas2wbY</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Miyoshi, Kentaroh, MD</creator><creator>Oto, Takahiro, MD</creator><creator>Otani, Shinji, MD</creator><creator>Tanaka, Shin, MD</creator><creator>Harada, Masaaki, MD</creator><creator>Kakishita, Tomokazu, MD</creator><creator>Hori, Shiro, MD</creator><creator>Waki, Naohisa, MD</creator><creator>Yamane, Masaomi, MD</creator><creator>Miyoshi, Shinichiro, MD</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>20110401</creationdate><title>Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation</title><author>Miyoshi, Kentaroh, MD ; Oto, Takahiro, MD ; Otani, Shinji, MD ; Tanaka, Shin, MD ; Harada, Masaaki, MD ; Kakishita, Tomokazu, MD ; Hori, Shiro, MD ; Waki, Naohisa, MD ; Yamane, Masaomi, MD ; Miyoshi, Shinichiro, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-47f9f69184537bf7d62454fda9f9b2403978ca72a0f2db88022f0c3678a69ae43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Death</topic><topic>definition</topic><topic>donation after cardiac death (DCD)</topic><topic>hypotension</topic><topic>Hypotension - complications</topic><topic>hypoxia</topic><topic>Hypoxia - complications</topic><topic>Lung - physiopathology</topic><topic>Lung Transplantation</topic><topic>Medical sciences</topic><topic>Surgery</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>Swine</topic><topic>Warm Ischemia</topic><topic>warm ischemic time (WIT)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miyoshi, Kentaroh, MD</creatorcontrib><creatorcontrib>Oto, Takahiro, MD</creatorcontrib><creatorcontrib>Otani, Shinji, MD</creatorcontrib><creatorcontrib>Tanaka, Shin, MD</creatorcontrib><creatorcontrib>Harada, Masaaki, MD</creatorcontrib><creatorcontrib>Kakishita, Tomokazu, MD</creatorcontrib><creatorcontrib>Hori, Shiro, MD</creatorcontrib><creatorcontrib>Waki, Naohisa, MD</creatorcontrib><creatorcontrib>Yamane, Masaomi, MD</creatorcontrib><creatorcontrib>Miyoshi, Shinichiro, MD</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>MEDLINE - Academic</collection><jtitle>The Journal of heart and lung transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miyoshi, Kentaroh, MD</au><au>Oto, Takahiro, MD</au><au>Otani, Shinji, MD</au><au>Tanaka, Shin, MD</au><au>Harada, Masaaki, MD</au><au>Kakishita, Tomokazu, MD</au><au>Hori, Shiro, MD</au><au>Waki, Naohisa, MD</au><au>Yamane, Masaomi, MD</au><au>Miyoshi, Shinichiro, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation</atitle><jtitle>The Journal of heart and lung transplantation</jtitle><addtitle>J Heart Lung Transplant</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>30</volume><issue>4</issue><spage>445</spage><epage>451</epage><pages>445-451</pages><issn>1053-2498</issn><eissn>1557-3117</eissn><abstract>Background The start of warm ischemic time (WIT) of donor lungs in donation after cardiac death (DCD) is not clearly defined. We investigated the effect of donor pre-mortem hypotension and hypoxia to determine which physiologic factor is the determinant of WIT onset in controlled DCD lung transplantation. Methods Twenty mechanically-ventilated donor pigs were placed in 4 groups ( n = 5 each) and exposed to each of the pseudo-agonal conditions for 60 minutes: (1) control group, no intervention and optimum ventilation, followed by cardiac arrest; (2) hypotension (HT) group, controlled cardiac tamponade reducing systolic blood pressure to <50 mm Hg, followed by cardiac arrest; (3) hypoventilation (HV) group, ventilation with room air at 5 breaths/min, followed by cardiac arrest; (4) non-circulation (NC) group, initial cardiac arrest, followed by a 60-minute standoff time. The lung graft was retrieved and the left lung was transplanted to the recipient. Graft function was evaluated for 4 hours after contralateral pulmonary artery ligation. The reperfusion injury was evaluated based on tissue cytokine expression, wet weight-to-dry weight ratio, and histology at the end of the reperfusion period. Results Impaired post-transplant graft function was seen in the HV group, which had significantly poorer oxygenation during the reperfusion period than the other groups ( p < 0.001). The HV group also had higher tissue levels of interleukin-8 ( p < 0.05), a higher wet weight-to-dry weight ratio ( p < 0.05), and histologic findings of graft tissue injury than the control group. The difference in these parameters among the control, HT, and NC groups was not significant. Conclusions Only pre-mortem hypoxia provoked by hypoventilation significantly impaired lung graft function in DCD lung transplantation. Ventilatory rather than circulatory deterioration can trigger the onset of warm ischemia.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>21211993</pmid><doi>10.1016/j.healun.2010.11.010</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Cardiology. Vascular system Death definition donation after cardiac death (DCD) hypotension Hypotension - complications hypoxia Hypoxia - complications Lung - physiopathology Lung Transplantation Medical sciences Surgery Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Swine Warm Ischemia warm ischemic time (WIT) |
title | Effect of donor pre-mortem hypoxia and hypotension on graft function and start of warm ischemia in donation after cardiac death lung transplantation |
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