Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo
Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal i...
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| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2003-12, Vol.18 (12), p.2629-2637 |
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| creator | Zareie, Mohammad Hekking, Liesbeth H. P. Welten, Angelique G. A. Driesprong, Bas A. J. Schadee-Eestermans, Inge L. Faict, Dirk Leyssens, Anne Schalkwijk, Casper G. Beelen, Robert H. J. ter Wee, Piet M. van den Born, Jacob |
| description | Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. Methods. Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. Results. The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P |
| doi_str_mv | 10.1093/ndt/gfg356 |
| format | Article |
| fullrecord | <record><control><sourceid>istex_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1093_ndt_gfg356</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_HXZ_XDF1FZX2_S</sourcerecordid><originalsourceid>FETCH-LOGICAL-c455t-602632301b71f16ade8fe6aa3ae662b5767f6a1aba9249a35a36947e31b0906d3</originalsourceid><addsrcrecordid>eNpF0EFLwzAUB_AgipvTix9AcvEi1iVNk7ZHmc4JAw8qjF3Ca5uUzq4ZSTrct7ezYzu9B__fe4c_QreUPFGSsnFT-HGpS8bFGRrSSJAgZAk_R8MupAHhJB2gK-dWhJA0jONLNNgjHibJEKmJabytstZXpsFG4xpyD17hrNVa2Udc1m1unMLQFMe9UKWFAv5PNtYUbe4d9gZvlK28aRTUuGpWrd11A2-rrblGFxpqp24Oc4S-p69fk1kw_3h7nzzPgzzi3AeChIKFjNAsppoKKFSilQBgoIQIMx6LWAugkEEaRikwDkykUawYzUhKRMFG6KH_m1vjnFVabmy1BruTlMh9V7LrSvZddfiux5s2W6viRA_ldOD-AMDlUGsLTV65k-tQlIq4c0HvKufV7zEH-yO7NOZytljKxcuUTpeLUH6yP8Vbg3I</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo</title><source>MEDLINE</source><source>Oxford University Press</source><source>Alma/SFX Local Collection</source><source>EZB Electronic Journals Library</source><creator>Zareie, Mohammad ; Hekking, Liesbeth H. P. ; Welten, Angelique G. A. ; Driesprong, Bas A. J. ; Schadee-Eestermans, Inge L. ; Faict, Dirk ; Leyssens, Anne ; Schalkwijk, Casper G. ; Beelen, Robert H. J. ; ter Wee, Piet M. ; van den Born, Jacob</creator><creatorcontrib>Zareie, Mohammad ; Hekking, Liesbeth H. P. ; Welten, Angelique G. A. ; Driesprong, Bas A. J. ; Schadee-Eestermans, Inge L. ; Faict, Dirk ; Leyssens, Anne ; Schalkwijk, Casper G. ; Beelen, Robert H. J. ; ter Wee, Piet M. ; van den Born, Jacob</creatorcontrib><description>Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. Methods. Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. Results. The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P < 0.03) and caused profound mesothelial damage. The vessel density in the omentum and the mesentery was significantly correlated to both the number of tissue mast cells and the hyaluronan content in the peritoneal lavage, which might suggest a role for mast cells and hyaluronan in the induction of angiogenesis. Conclusions. Instillations of low pH lactate buffer, a high glucose concentration and glucose degradation products contribute differently and often cumulatively to peritoneal injury in vivo.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfg356</identifier><identifier>PMID: 14605288</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Buffers ; CAPD ; Dialysis Solutions - adverse effects ; Emergency and intensive care: renal failure. Dialysis management ; glucose ; Glucose - adverse effects ; glucose degradation products ; Glycation End Products, Advanced ; Hydrogen-Ion Concentration ; Intensive care medicine ; lactate buffer ; Lactic Acid - adverse effects ; Male ; Medical sciences ; Models, Animal ; Omentum - pathology ; Peritoneal Dialysis, Continuous Ambulatory - adverse effects ; Peritoneal Dialysis, Continuous Ambulatory - methods ; Peritoneal Diseases - etiology ; Peritoneal Diseases - pathology ; peritoneal injury ; Peritoneum - pathology ; Rats ; Rats, Wistar</subject><ispartof>Nephrology, dialysis, transplantation, 2003-12, Vol.18 (12), p.2629-2637</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-602632301b71f16ade8fe6aa3ae662b5767f6a1aba9249a35a36947e31b0906d3</citedby><cites>FETCH-LOGICAL-c455t-602632301b71f16ade8fe6aa3ae662b5767f6a1aba9249a35a36947e31b0906d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15284967$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14605288$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zareie, Mohammad</creatorcontrib><creatorcontrib>Hekking, Liesbeth H. P.</creatorcontrib><creatorcontrib>Welten, Angelique G. A.</creatorcontrib><creatorcontrib>Driesprong, Bas A. J.</creatorcontrib><creatorcontrib>Schadee-Eestermans, Inge L.</creatorcontrib><creatorcontrib>Faict, Dirk</creatorcontrib><creatorcontrib>Leyssens, Anne</creatorcontrib><creatorcontrib>Schalkwijk, Casper G.</creatorcontrib><creatorcontrib>Beelen, Robert H. J.</creatorcontrib><creatorcontrib>ter Wee, Piet M.</creatorcontrib><creatorcontrib>van den Born, Jacob</creatorcontrib><title>Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol. Dial. Transplant</addtitle><description>Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. Methods. Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. Results. The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P < 0.03) and caused profound mesothelial damage. The vessel density in the omentum and the mesentery was significantly correlated to both the number of tissue mast cells and the hyaluronan content in the peritoneal lavage, which might suggest a role for mast cells and hyaluronan in the induction of angiogenesis. Conclusions. Instillations of low pH lactate buffer, a high glucose concentration and glucose degradation products contribute differently and often cumulatively to peritoneal injury in vivo.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Buffers</subject><subject>CAPD</subject><subject>Dialysis Solutions - adverse effects</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>glucose</subject><subject>Glucose - adverse effects</subject><subject>glucose degradation products</subject><subject>Glycation End Products, Advanced</subject><subject>Hydrogen-Ion Concentration</subject><subject>Intensive care medicine</subject><subject>lactate buffer</subject><subject>Lactic Acid - adverse effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Animal</subject><subject>Omentum - pathology</subject><subject>Peritoneal Dialysis, Continuous Ambulatory - adverse effects</subject><subject>Peritoneal Dialysis, Continuous Ambulatory - methods</subject><subject>Peritoneal Diseases - etiology</subject><subject>Peritoneal Diseases - pathology</subject><subject>peritoneal injury</subject><subject>Peritoneum - pathology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0EFLwzAUB_AgipvTix9AcvEi1iVNk7ZHmc4JAw8qjF3Ca5uUzq4ZSTrct7ezYzu9B__fe4c_QreUPFGSsnFT-HGpS8bFGRrSSJAgZAk_R8MupAHhJB2gK-dWhJA0jONLNNgjHibJEKmJabytstZXpsFG4xpyD17hrNVa2Udc1m1unMLQFMe9UKWFAv5PNtYUbe4d9gZvlK28aRTUuGpWrd11A2-rrblGFxpqp24Oc4S-p69fk1kw_3h7nzzPgzzi3AeChIKFjNAsppoKKFSilQBgoIQIMx6LWAugkEEaRikwDkykUawYzUhKRMFG6KH_m1vjnFVabmy1BruTlMh9V7LrSvZddfiux5s2W6viRA_ldOD-AMDlUGsLTV65k-tQlIq4c0HvKufV7zEH-yO7NOZytljKxcuUTpeLUH6yP8Vbg3I</recordid><startdate>20031201</startdate><enddate>20031201</enddate><creator>Zareie, Mohammad</creator><creator>Hekking, Liesbeth H. P.</creator><creator>Welten, Angelique G. A.</creator><creator>Driesprong, Bas A. J.</creator><creator>Schadee-Eestermans, Inge L.</creator><creator>Faict, Dirk</creator><creator>Leyssens, Anne</creator><creator>Schalkwijk, Casper G.</creator><creator>Beelen, Robert H. J.</creator><creator>ter Wee, Piet M.</creator><creator>van den Born, Jacob</creator><general>Oxford University Press</general><scope>BSCLL</scope><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></search><sort><creationdate>20031201</creationdate><title>Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo</title><author>Zareie, Mohammad ; Hekking, Liesbeth H. P. ; Welten, Angelique G. A. ; Driesprong, Bas A. J. ; Schadee-Eestermans, Inge L. ; Faict, Dirk ; Leyssens, Anne ; Schalkwijk, Casper G. ; Beelen, Robert H. 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Dialysis management</topic><topic>glucose</topic><topic>Glucose - adverse effects</topic><topic>glucose degradation products</topic><topic>Glycation End Products, Advanced</topic><topic>Hydrogen-Ion Concentration</topic><topic>Intensive care medicine</topic><topic>lactate buffer</topic><topic>Lactic Acid - adverse effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Animal</topic><topic>Omentum - pathology</topic><topic>Peritoneal Dialysis, Continuous Ambulatory - adverse effects</topic><topic>Peritoneal Dialysis, Continuous Ambulatory - methods</topic><topic>Peritoneal Diseases - etiology</topic><topic>Peritoneal Diseases - pathology</topic><topic>peritoneal injury</topic><topic>Peritoneum - pathology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zareie, Mohammad</creatorcontrib><creatorcontrib>Hekking, Liesbeth H. P.</creatorcontrib><creatorcontrib>Welten, Angelique G. A.</creatorcontrib><creatorcontrib>Driesprong, Bas A. J.</creatorcontrib><creatorcontrib>Schadee-Eestermans, Inge L.</creatorcontrib><creatorcontrib>Faict, Dirk</creatorcontrib><creatorcontrib>Leyssens, Anne</creatorcontrib><creatorcontrib>Schalkwijk, Casper G.</creatorcontrib><creatorcontrib>Beelen, Robert H. J.</creatorcontrib><creatorcontrib>ter Wee, Piet M.</creatorcontrib><creatorcontrib>van den Born, Jacob</creatorcontrib><collection>Istex</collection><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><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zareie, Mohammad</au><au>Hekking, Liesbeth H. P.</au><au>Welten, Angelique G. A.</au><au>Driesprong, Bas A. J.</au><au>Schadee-Eestermans, Inge L.</au><au>Faict, Dirk</au><au>Leyssens, Anne</au><au>Schalkwijk, Casper G.</au><au>Beelen, Robert H. J.</au><au>ter Wee, Piet M.</au><au>van den Born, Jacob</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><addtitle>Nephrol. Dial. Transplant</addtitle><date>2003-12-01</date><risdate>2003</risdate><volume>18</volume><issue>12</issue><spage>2629</spage><epage>2637</epage><pages>2629-2637</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. Methods. Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. Results. The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P < 0.03) and caused profound mesothelial damage. The vessel density in the omentum and the mesentery was significantly correlated to both the number of tissue mast cells and the hyaluronan content in the peritoneal lavage, which might suggest a role for mast cells and hyaluronan in the induction of angiogenesis. Conclusions. Instillations of low pH lactate buffer, a high glucose concentration and glucose degradation products contribute differently and often cumulatively to peritoneal injury in vivo.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>14605288</pmid><doi>10.1093/ndt/gfg356</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Buffers CAPD Dialysis Solutions - adverse effects Emergency and intensive care: renal failure. Dialysis management glucose Glucose - adverse effects glucose degradation products Glycation End Products, Advanced Hydrogen-Ion Concentration Intensive care medicine lactate buffer Lactic Acid - adverse effects Male Medical sciences Models, Animal Omentum - pathology Peritoneal Dialysis, Continuous Ambulatory - adverse effects Peritoneal Dialysis, Continuous Ambulatory - methods Peritoneal Diseases - etiology Peritoneal Diseases - pathology peritoneal injury Peritoneum - pathology Rats Rats, Wistar |
| title | Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo |
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