Hyaluronic acid secretion during carbon dioxide pneumoperitoneum and its association with port-site metastasis in a murine model
The mechanism of port-site metastasis after laparoscopic cancer surgery is unclear. This study aimed to determine whether carbon dioxide (CO2) pneumoperitoneum caused an increase in hyaluronic acid, which is secreted from mesothelial cells of the peritoneal cavity, and to assess the risk for port-si...
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Veröffentlicht in: | Surgical endoscopy 2001, Vol.15 (1), p.59-62 |
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description | The mechanism of port-site metastasis after laparoscopic cancer surgery is unclear. This study aimed to determine whether carbon dioxide (CO2) pneumoperitoneum caused an increase in hyaluronic acid, which is secreted from mesothelial cells of the peritoneal cavity, and to assess the risk for port-site metastasis using a murine pneumoperitoneal model.
Sandwich-binding protein assay was used to measure the concentration of hyaluronic acid in the peritoneal cavity at 6, 12, 18, 24, 48, and 72 h after CO2 pneumoperitoneum or laparotomy for 30 min. The concentrations of hyaluronic acid during pneumoperitoneum were compared among different gases (CO2, helium, air), intervals (5, 30, 60 min), and pressures (0-2, 4-6, 8-10 mmHg). To investigate the effects of exogenous hyaluronic acid, the development of port-site metastasis was examined using mouse adenocarcinoma cell-line colon 26 cells.
The intraperitoneal concentration of hyaluronic acid after CO2 pneumoperitoneum had increased already at 6 h, had reached the maximum level at 24 h, and had begun to decrease at 72 h. The concentration of hyaluronic acid at 24 h and 48 h in the CO2 pneumoperitoneum group was higher than that in the laparotomy group. This increase in hyaluronic acid also was found during helium and air pneumoperitoneum, and the concentration of hyaluronic acid in the peritoneal cavity was at its maximum when CO2 pneumoperitoneum lasted 30 min at 4 to 6 mmHg. The frequency of port-site metastasis was the highest when hyaluronic acid was injected during CO2 pneumoperitoneum (100%).
In a murine model, the intraperitoneal concentration of hyaluronic acid was significantly increased after CO2 pneumoperitoneum, and the increase was more evident than that after laparotomy. Increased hyaluronic acid during pneumoperitoneum may be associated with port-site metastasis after laparoscopic cancer surgery. |
doi_str_mv | 10.1007/s004640000238 |
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Sandwich-binding protein assay was used to measure the concentration of hyaluronic acid in the peritoneal cavity at 6, 12, 18, 24, 48, and 72 h after CO2 pneumoperitoneum or laparotomy for 30 min. The concentrations of hyaluronic acid during pneumoperitoneum were compared among different gases (CO2, helium, air), intervals (5, 30, 60 min), and pressures (0-2, 4-6, 8-10 mmHg). To investigate the effects of exogenous hyaluronic acid, the development of port-site metastasis was examined using mouse adenocarcinoma cell-line colon 26 cells.
The intraperitoneal concentration of hyaluronic acid after CO2 pneumoperitoneum had increased already at 6 h, had reached the maximum level at 24 h, and had begun to decrease at 72 h. The concentration of hyaluronic acid at 24 h and 48 h in the CO2 pneumoperitoneum group was higher than that in the laparotomy group. This increase in hyaluronic acid also was found during helium and air pneumoperitoneum, and the concentration of hyaluronic acid in the peritoneal cavity was at its maximum when CO2 pneumoperitoneum lasted 30 min at 4 to 6 mmHg. The frequency of port-site metastasis was the highest when hyaluronic acid was injected during CO2 pneumoperitoneum (100%).
In a murine model, the intraperitoneal concentration of hyaluronic acid was significantly increased after CO2 pneumoperitoneum, and the increase was more evident than that after laparotomy. Increased hyaluronic acid during pneumoperitoneum may be associated with port-site metastasis after laparoscopic cancer surgery.</description><identifier>ISSN: 0930-2794</identifier><identifier>EISSN: 1432-2218</identifier><identifier>DOI: 10.1007/s004640000238</identifier><identifier>PMID: 11178765</identifier><identifier>CODEN: SUREEX</identifier><language>eng</language><publisher>New York, NY: Springer</publisher><subject>Abdomen ; Adenocarcinoma - metabolism ; Animals ; Biological and medical sciences ; Cancer surgery ; Carbon dioxide ; Colonic Neoplasms - metabolism ; Hyaluronic acid ; Hyaluronic Acid - metabolism ; Laparoscopy ; Laparotomy ; Male ; Medical research ; Medical sciences ; Metastasis ; Mice ; Mice, Inbred BALB C ; Models, Animal ; Neoplasm Seeding ; Peritoneum - metabolism ; Pneumoperitoneum, Artificial ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the digestive system ; Tumor Cells, Cultured</subject><ispartof>Surgical endoscopy, 2001, Vol.15 (1), p.59-62</ispartof><rights>2001 INIST-CNRS</rights><rights>Springer-Verlag 2001</rights><rights>Springer-Verlag 2001.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-5094c85e3ed7414161be4f4a04131d300783dfabcefeddefd54921275f5a47ed3</citedby><cites>FETCH-LOGICAL-c372t-5094c85e3ed7414161be4f4a04131d300783dfabcefeddefd54921275f5a47ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=915112$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11178765$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YAMAGUCHI, K</creatorcontrib><creatorcontrib>HIRABAYASHI, Y</creatorcontrib><creatorcontrib>SUEMATSU, T</creatorcontrib><creatorcontrib>SHIRAISHI, N</creatorcontrib><creatorcontrib>ADACHI, Y</creatorcontrib><creatorcontrib>KITANO, S</creatorcontrib><title>Hyaluronic acid secretion during carbon dioxide pneumoperitoneum and its association with port-site metastasis in a murine model</title><title>Surgical endoscopy</title><addtitle>Surg Endosc</addtitle><description>The mechanism of port-site metastasis after laparoscopic cancer surgery is unclear. This study aimed to determine whether carbon dioxide (CO2) pneumoperitoneum caused an increase in hyaluronic acid, which is secreted from mesothelial cells of the peritoneal cavity, and to assess the risk for port-site metastasis using a murine pneumoperitoneal model.
Sandwich-binding protein assay was used to measure the concentration of hyaluronic acid in the peritoneal cavity at 6, 12, 18, 24, 48, and 72 h after CO2 pneumoperitoneum or laparotomy for 30 min. The concentrations of hyaluronic acid during pneumoperitoneum were compared among different gases (CO2, helium, air), intervals (5, 30, 60 min), and pressures (0-2, 4-6, 8-10 mmHg). To investigate the effects of exogenous hyaluronic acid, the development of port-site metastasis was examined using mouse adenocarcinoma cell-line colon 26 cells.
The intraperitoneal concentration of hyaluronic acid after CO2 pneumoperitoneum had increased already at 6 h, had reached the maximum level at 24 h, and had begun to decrease at 72 h. The concentration of hyaluronic acid at 24 h and 48 h in the CO2 pneumoperitoneum group was higher than that in the laparotomy group. This increase in hyaluronic acid also was found during helium and air pneumoperitoneum, and the concentration of hyaluronic acid in the peritoneal cavity was at its maximum when CO2 pneumoperitoneum lasted 30 min at 4 to 6 mmHg. The frequency of port-site metastasis was the highest when hyaluronic acid was injected during CO2 pneumoperitoneum (100%).
In a murine model, the intraperitoneal concentration of hyaluronic acid was significantly increased after CO2 pneumoperitoneum, and the increase was more evident than that after laparotomy. Increased hyaluronic acid during pneumoperitoneum may be associated with port-site metastasis after laparoscopic cancer surgery.</description><subject>Abdomen</subject><subject>Adenocarcinoma - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cancer surgery</subject><subject>Carbon dioxide</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Hyaluronic acid</subject><subject>Hyaluronic Acid - metabolism</subject><subject>Laparoscopy</subject><subject>Laparotomy</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Models, Animal</subject><subject>Neoplasm Seeding</subject><subject>Peritoneum - metabolism</subject><subject>Pneumoperitoneum, Artificial</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the digestive system</subject><subject>Tumor Cells, Cultured</subject><issn>0930-2794</issn><issn>1432-2218</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp10ctrFTEUB-Agir1Wl24lKLibmpPHZGYpRa1Q6EbXQ25yRlNmJmNOBu3OP7259uILGgJ58OVwyI-x5yDOQAj7hoTQrRZ1SNU9YDvQSjZSQveQ7USvRCNtr0_YE6LranQP5jE7AQDb2dbs2M-LGzdtOS3Rc-dj4IQ-Y4lp4WHLcfnCvcv7wymmHzEgXxfc5rRijiUdttwtgcdC3BElH92vp99j-crXlEtDsSCfsTiqMxKPC3d8PlSu1yng9JQ9Gt1E-Oy4nrLP7999Or9oLq8-fDx_e9l4ZWVpjOi17wwqDFaDhhb2qEfthAYFQdWf6FQY3d7jiCHgGIzuJUhrRuO0xaBO2eu7umtO3zakMsyRPE6TWzBtNFhhrBVtW-Gr_-B12vJSextk_TStRaf7ql7eq6CvAIypqLlDPieijOOw5ji7fDOAGA7pDf-kV_2LY9FtP2P4o49x_dWbI--mMbvFR_rtargAUt0CzkWifw</recordid><startdate>2001</startdate><enddate>2001</enddate><creator>YAMAGUCHI, K</creator><creator>HIRABAYASHI, Y</creator><creator>SUEMATSU, T</creator><creator>SHIRAISHI, N</creator><creator>ADACHI, Y</creator><creator>KITANO, S</creator><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>2001</creationdate><title>Hyaluronic acid secretion during carbon dioxide pneumoperitoneum and its association with port-site metastasis in a murine model</title><author>YAMAGUCHI, K ; HIRABAYASHI, Y ; SUEMATSU, T ; SHIRAISHI, N ; ADACHI, Y ; KITANO, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-5094c85e3ed7414161be4f4a04131d300783dfabcefeddefd54921275f5a47ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Abdomen</topic><topic>Adenocarcinoma - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cancer surgery</topic><topic>Carbon dioxide</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Hyaluronic acid</topic><topic>Hyaluronic Acid - metabolism</topic><topic>Laparoscopy</topic><topic>Laparotomy</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Models, Animal</topic><topic>Neoplasm Seeding</topic><topic>Peritoneum - metabolism</topic><topic>Pneumoperitoneum, Artificial</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the digestive system</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YAMAGUCHI, K</creatorcontrib><creatorcontrib>HIRABAYASHI, Y</creatorcontrib><creatorcontrib>SUEMATSU, T</creatorcontrib><creatorcontrib>SHIRAISHI, N</creatorcontrib><creatorcontrib>ADACHI, Y</creatorcontrib><creatorcontrib>KITANO, S</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Surgical endoscopy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YAMAGUCHI, K</au><au>HIRABAYASHI, Y</au><au>SUEMATSU, T</au><au>SHIRAISHI, N</au><au>ADACHI, Y</au><au>KITANO, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyaluronic acid secretion during carbon dioxide pneumoperitoneum and its association with port-site metastasis in a murine model</atitle><jtitle>Surgical endoscopy</jtitle><addtitle>Surg Endosc</addtitle><date>2001</date><risdate>2001</risdate><volume>15</volume><issue>1</issue><spage>59</spage><epage>62</epage><pages>59-62</pages><issn>0930-2794</issn><eissn>1432-2218</eissn><coden>SUREEX</coden><abstract>The mechanism of port-site metastasis after laparoscopic cancer surgery is unclear. This study aimed to determine whether carbon dioxide (CO2) pneumoperitoneum caused an increase in hyaluronic acid, which is secreted from mesothelial cells of the peritoneal cavity, and to assess the risk for port-site metastasis using a murine pneumoperitoneal model.
Sandwich-binding protein assay was used to measure the concentration of hyaluronic acid in the peritoneal cavity at 6, 12, 18, 24, 48, and 72 h after CO2 pneumoperitoneum or laparotomy for 30 min. The concentrations of hyaluronic acid during pneumoperitoneum were compared among different gases (CO2, helium, air), intervals (5, 30, 60 min), and pressures (0-2, 4-6, 8-10 mmHg). To investigate the effects of exogenous hyaluronic acid, the development of port-site metastasis was examined using mouse adenocarcinoma cell-line colon 26 cells.
The intraperitoneal concentration of hyaluronic acid after CO2 pneumoperitoneum had increased already at 6 h, had reached the maximum level at 24 h, and had begun to decrease at 72 h. The concentration of hyaluronic acid at 24 h and 48 h in the CO2 pneumoperitoneum group was higher than that in the laparotomy group. This increase in hyaluronic acid also was found during helium and air pneumoperitoneum, and the concentration of hyaluronic acid in the peritoneal cavity was at its maximum when CO2 pneumoperitoneum lasted 30 min at 4 to 6 mmHg. The frequency of port-site metastasis was the highest when hyaluronic acid was injected during CO2 pneumoperitoneum (100%).
In a murine model, the intraperitoneal concentration of hyaluronic acid was significantly increased after CO2 pneumoperitoneum, and the increase was more evident than that after laparotomy. Increased hyaluronic acid during pneumoperitoneum may be associated with port-site metastasis after laparoscopic cancer surgery.</abstract><cop>New York, NY</cop><pub>Springer</pub><pmid>11178765</pmid><doi>10.1007/s004640000238</doi><tpages>4</tpages></addata></record> |
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subjects | Abdomen Adenocarcinoma - metabolism Animals Biological and medical sciences Cancer surgery Carbon dioxide Colonic Neoplasms - metabolism Hyaluronic acid Hyaluronic Acid - metabolism Laparoscopy Laparotomy Male Medical research Medical sciences Metastasis Mice Mice, Inbred BALB C Models, Animal Neoplasm Seeding Peritoneum - metabolism Pneumoperitoneum, Artificial Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the digestive system Tumor Cells, Cultured |
title | Hyaluronic acid secretion during carbon dioxide pneumoperitoneum and its association with port-site metastasis in a murine model |
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