Reduction of Post-surgical Pericardial Adhesions Using a Pig Model

Background Post-surgical pericardial adhesions pose an increased risk of complications during redo sternotomies. Adhesive tissue formation is a normal response to tissue injury and involves complex patho-physiological processes including the actions of prostaglandins to cause plasma leakage and fibr...

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Veröffentlicht in:Heart, lung & circulation lung & circulation, 2012-01, Vol.21 (1), p.22-29
Hauptverfasser: Alizzi, Ali M., MD, Summers, Phillip, PhD, Boon, Virginia H., BPharm (Hons), Tantiongco, John-Paul, BMBS, Thompson, Teresa, BN, Leslie, Belinda J., BVSc, Williams, David, FRCPath, Steele, Mike, PhD, Bidstrup, Benjamin P., FRACS, Diqer, Al-Mutazz A., FRACs
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container_end_page 29
container_issue 1
container_start_page 22
container_title Heart, lung & circulation
container_volume 21
creator Alizzi, Ali M., MD
Summers, Phillip, PhD
Boon, Virginia H., BPharm (Hons)
Tantiongco, John-Paul, BMBS
Thompson, Teresa, BN
Leslie, Belinda J., BVSc
Williams, David, FRCPath
Steele, Mike, PhD
Bidstrup, Benjamin P., FRACS
Diqer, Al-Mutazz A., FRACs
description Background Post-surgical pericardial adhesions pose an increased risk of complications during redo sternotomies. Adhesive tissue formation is a normal response to tissue injury and involves complex patho-physiological processes including the actions of prostaglandins to cause plasma leakage and fibrin formation. The purpose of this study was to assess the ability of two non-steroidal anti-inflammatory agents (Indomethacin and Rofecoxib) and a barrier (Coseal, a polyethylene glycol) to limit adhesion formation following cardiac surgery in a pig model. Methods Forty-four piglets were allocated equally to four treatment groups: Group 1: Control, Group 2: intramuscular Indomethacin, Group 3: oral Rofecoxib and Group 4: Coseal sprayed on the heart. A full median sternotomy was performed on each animal and the heart exposed. Adhesions were induced by rubbing tissues with gauze, applying sutures and leaving blood in the pericardial sac before chest closure. Plasma inflammatory markers including prostaglandin E2 and thromboxane B2 were measured preoperatively and on Days 2, 5 and 10 after surgery. Eight animals from each group were slaughtered after 12 weeks and 3 after 25 weeks. Adhesions were assessed macroscopically and microscopically. Results Compared to the Control group, the extent of adhesions was significantly less in all other groups whilst adhesion density was least in the Indomethacin and Coseal groups. Indomethacin and less so Rofecoxib, inhibited the synthesis of prostaglandin E2 and thromboxane B2 but there were no significant changes in other inflammatory markers. Conclusions We conclude that systemic Indomethacin, and locally applied Coseal are suitable methods to markedly reduce pericardial and retrosternal adhesions.
doi_str_mv 10.1016/j.hlc.2011.10.002
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Adhesive tissue formation is a normal response to tissue injury and involves complex patho-physiological processes including the actions of prostaglandins to cause plasma leakage and fibrin formation. The purpose of this study was to assess the ability of two non-steroidal anti-inflammatory agents (Indomethacin and Rofecoxib) and a barrier (Coseal, a polyethylene glycol) to limit adhesion formation following cardiac surgery in a pig model. Methods Forty-four piglets were allocated equally to four treatment groups: Group 1: Control, Group 2: intramuscular Indomethacin, Group 3: oral Rofecoxib and Group 4: Coseal sprayed on the heart. A full median sternotomy was performed on each animal and the heart exposed. Adhesions were induced by rubbing tissues with gauze, applying sutures and leaving blood in the pericardial sac before chest closure. Plasma inflammatory markers including prostaglandin E2 and thromboxane B2 were measured preoperatively and on Days 2, 5 and 10 after surgery. Eight animals from each group were slaughtered after 12 weeks and 3 after 25 weeks. Adhesions were assessed macroscopically and microscopically. Results Compared to the Control group, the extent of adhesions was significantly less in all other groups whilst adhesion density was least in the Indomethacin and Coseal groups. Indomethacin and less so Rofecoxib, inhibited the synthesis of prostaglandin E2 and thromboxane B2 but there were no significant changes in other inflammatory markers. Conclusions We conclude that systemic Indomethacin, and locally applied Coseal are suitable methods to markedly reduce pericardial and retrosternal adhesions.</description><identifier>ISSN: 1443-9506</identifier><identifier>EISSN: 1444-2892</identifier><identifier>DOI: 10.1016/j.hlc.2011.10.002</identifier><identifier>PMID: 22078313</identifier><language>eng</language><publisher>Australia: Elsevier B.V</publisher><subject><![CDATA[Adhesions ; Animal model ; Animals ; Biological Availability ; Biomarkers ; Cardiovascular ; Cyclooxygenase 2 Inhibitors - administration & dosage ; Cyclooxygenase 2 Inhibitors - pharmacokinetics ; Dinoprostone - blood ; Disease Models, Animal ; Drug Monitoring ; Indomethacin - administration & dosage ; Indomethacin - pharmacokinetics ; Inflammation ; Inflammation - blood ; Lactones - administration & dosage ; Lactones - pharmacokinetics ; Pericardium ; Pericardium - drug effects ; Pericardium - pathology ; Perioperative Period - methods ; Polyethylene Glycols - administration & dosage ; Polyethylene Glycols - pharmacokinetics ; Postoperative Complications - blood ; Postoperative Complications - etiology ; Postoperative Complications - prevention & control ; Prostaglandins ; Sternotomy - adverse effects ; Sternotomy - methods ; Sulfones - administration & dosage ; Sulfones - pharmacokinetics ; Surface-Active Agents - administration & dosage ; Surface-Active Agents - pharmacokinetics ; Swine ; Thromboxane B2 - blood ; Tissue Adhesions - blood ; Tissue Adhesions - etiology ; Tissue Adhesions - pathology ; Tissue Adhesions - prevention & control ; Treatment Outcome]]></subject><ispartof>Heart, lung &amp; circulation, 2012-01, Vol.21 (1), p.22-29</ispartof><rights>Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand</rights><rights>2011 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand</rights><rights>Copyright © 2011 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-f0501b515bc87104cb7bf6c4b6ef56c0b941714460fc3834f5efa48cd6b97dff3</citedby><cites>FETCH-LOGICAL-c516t-f0501b515bc87104cb7bf6c4b6ef56c0b941714460fc3834f5efa48cd6b97dff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1443950611012066$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22078313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alizzi, Ali M., MD</creatorcontrib><creatorcontrib>Summers, Phillip, PhD</creatorcontrib><creatorcontrib>Boon, Virginia H., BPharm (Hons)</creatorcontrib><creatorcontrib>Tantiongco, John-Paul, BMBS</creatorcontrib><creatorcontrib>Thompson, Teresa, BN</creatorcontrib><creatorcontrib>Leslie, Belinda J., BVSc</creatorcontrib><creatorcontrib>Williams, David, FRCPath</creatorcontrib><creatorcontrib>Steele, Mike, PhD</creatorcontrib><creatorcontrib>Bidstrup, Benjamin P., FRACS</creatorcontrib><creatorcontrib>Diqer, Al-Mutazz A., FRACs</creatorcontrib><title>Reduction of Post-surgical Pericardial Adhesions Using a Pig Model</title><title>Heart, lung &amp; circulation</title><addtitle>Heart Lung Circ</addtitle><description>Background Post-surgical pericardial adhesions pose an increased risk of complications during redo sternotomies. Adhesive tissue formation is a normal response to tissue injury and involves complex patho-physiological processes including the actions of prostaglandins to cause plasma leakage and fibrin formation. The purpose of this study was to assess the ability of two non-steroidal anti-inflammatory agents (Indomethacin and Rofecoxib) and a barrier (Coseal, a polyethylene glycol) to limit adhesion formation following cardiac surgery in a pig model. Methods Forty-four piglets were allocated equally to four treatment groups: Group 1: Control, Group 2: intramuscular Indomethacin, Group 3: oral Rofecoxib and Group 4: Coseal sprayed on the heart. A full median sternotomy was performed on each animal and the heart exposed. Adhesions were induced by rubbing tissues with gauze, applying sutures and leaving blood in the pericardial sac before chest closure. Plasma inflammatory markers including prostaglandin E2 and thromboxane B2 were measured preoperatively and on Days 2, 5 and 10 after surgery. Eight animals from each group were slaughtered after 12 weeks and 3 after 25 weeks. Adhesions were assessed macroscopically and microscopically. Results Compared to the Control group, the extent of adhesions was significantly less in all other groups whilst adhesion density was least in the Indomethacin and Coseal groups. Indomethacin and less so Rofecoxib, inhibited the synthesis of prostaglandin E2 and thromboxane B2 but there were no significant changes in other inflammatory markers. Conclusions We conclude that systemic Indomethacin, and locally applied Coseal are suitable methods to markedly reduce pericardial and retrosternal adhesions.</description><subject>Adhesions</subject><subject>Animal model</subject><subject>Animals</subject><subject>Biological Availability</subject><subject>Biomarkers</subject><subject>Cardiovascular</subject><subject>Cyclooxygenase 2 Inhibitors - administration &amp; dosage</subject><subject>Cyclooxygenase 2 Inhibitors - pharmacokinetics</subject><subject>Dinoprostone - blood</subject><subject>Disease Models, Animal</subject><subject>Drug Monitoring</subject><subject>Indomethacin - administration &amp; dosage</subject><subject>Indomethacin - pharmacokinetics</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Lactones - administration &amp; dosage</subject><subject>Lactones - pharmacokinetics</subject><subject>Pericardium</subject><subject>Pericardium - drug effects</subject><subject>Pericardium - pathology</subject><subject>Perioperative Period - methods</subject><subject>Polyethylene Glycols - administration &amp; dosage</subject><subject>Polyethylene Glycols - pharmacokinetics</subject><subject>Postoperative Complications - blood</subject><subject>Postoperative Complications - etiology</subject><subject>Postoperative Complications - prevention &amp; control</subject><subject>Prostaglandins</subject><subject>Sternotomy - adverse effects</subject><subject>Sternotomy - methods</subject><subject>Sulfones - administration &amp; dosage</subject><subject>Sulfones - pharmacokinetics</subject><subject>Surface-Active Agents - administration &amp; dosage</subject><subject>Surface-Active Agents - pharmacokinetics</subject><subject>Swine</subject><subject>Thromboxane B2 - blood</subject><subject>Tissue Adhesions - blood</subject><subject>Tissue Adhesions - etiology</subject><subject>Tissue Adhesions - pathology</subject><subject>Tissue Adhesions - prevention &amp; control</subject><subject>Treatment Outcome</subject><issn>1443-9506</issn><issn>1444-2892</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9P3DAQxa2qiD9bPkAvVW6csp1JHCdRJSS6aikSiBVlz1ZijxdvszHYCRLfvg675cChpxlb7z3N_IaxzwhzBBRfN_OHTs0zQIzvOUD2gR0j5zzNqjr7-NrnaV2AOGInIWwAsOR5fciOsgzKKsf8mH2_Iz2qwbo-cSZZujCkYfRrq5ouWZKP1Wsb-wv9QCGqQrIKtl8nTbK06-TGaeo-sQPTdIFO93XGVj9_3C9-pde3l1eLi-tUFSiG1EAB2BZYtKoqEbhqy9YIxVtBphAK2ppjGScWYFRe5dwUZBpeKS3autTG5DN2tst99O5ppDDIrQ2Kuq7pyY1B1igKrCGuNWO4UyrvQvBk5KO328a_SAQ5kZMbGcnJidz0FclFz5d9-thuSb85_qGKgm87AcUdny15GZSlXpG2ntQgtbP_jT9_51ad7SfMf-iFwsaNvo_wJMqQSZC_p9NNl8OYl4EQ-V_1L5IQ</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Alizzi, Ali M., MD</creator><creator>Summers, Phillip, PhD</creator><creator>Boon, Virginia H., BPharm (Hons)</creator><creator>Tantiongco, John-Paul, BMBS</creator><creator>Thompson, Teresa, BN</creator><creator>Leslie, Belinda J., BVSc</creator><creator>Williams, David, FRCPath</creator><creator>Steele, Mike, PhD</creator><creator>Bidstrup, Benjamin P., FRACS</creator><creator>Diqer, Al-Mutazz A., FRACs</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20120101</creationdate><title>Reduction of Post-surgical Pericardial Adhesions Using a Pig Model</title><author>Alizzi, Ali M., MD ; Summers, Phillip, PhD ; Boon, Virginia H., BPharm (Hons) ; Tantiongco, John-Paul, BMBS ; Thompson, Teresa, BN ; Leslie, Belinda J., BVSc ; Williams, David, FRCPath ; Steele, Mike, PhD ; Bidstrup, Benjamin P., FRACS ; Diqer, Al-Mutazz A., FRACs</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-f0501b515bc87104cb7bf6c4b6ef56c0b941714460fc3834f5efa48cd6b97dff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adhesions</topic><topic>Animal model</topic><topic>Animals</topic><topic>Biological Availability</topic><topic>Biomarkers</topic><topic>Cardiovascular</topic><topic>Cyclooxygenase 2 Inhibitors - administration &amp; dosage</topic><topic>Cyclooxygenase 2 Inhibitors - pharmacokinetics</topic><topic>Dinoprostone - blood</topic><topic>Disease Models, Animal</topic><topic>Drug Monitoring</topic><topic>Indomethacin - administration &amp; dosage</topic><topic>Indomethacin - pharmacokinetics</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Lactones - administration &amp; dosage</topic><topic>Lactones - pharmacokinetics</topic><topic>Pericardium</topic><topic>Pericardium - drug effects</topic><topic>Pericardium - pathology</topic><topic>Perioperative Period - methods</topic><topic>Polyethylene Glycols - administration &amp; dosage</topic><topic>Polyethylene Glycols - pharmacokinetics</topic><topic>Postoperative Complications - blood</topic><topic>Postoperative Complications - etiology</topic><topic>Postoperative Complications - prevention &amp; control</topic><topic>Prostaglandins</topic><topic>Sternotomy - adverse effects</topic><topic>Sternotomy - methods</topic><topic>Sulfones - administration &amp; dosage</topic><topic>Sulfones - pharmacokinetics</topic><topic>Surface-Active Agents - administration &amp; dosage</topic><topic>Surface-Active Agents - pharmacokinetics</topic><topic>Swine</topic><topic>Thromboxane B2 - blood</topic><topic>Tissue Adhesions - blood</topic><topic>Tissue Adhesions - etiology</topic><topic>Tissue Adhesions - pathology</topic><topic>Tissue Adhesions - prevention &amp; control</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alizzi, Ali M., MD</creatorcontrib><creatorcontrib>Summers, Phillip, PhD</creatorcontrib><creatorcontrib>Boon, Virginia H., BPharm (Hons)</creatorcontrib><creatorcontrib>Tantiongco, John-Paul, BMBS</creatorcontrib><creatorcontrib>Thompson, Teresa, BN</creatorcontrib><creatorcontrib>Leslie, Belinda J., BVSc</creatorcontrib><creatorcontrib>Williams, David, FRCPath</creatorcontrib><creatorcontrib>Steele, Mike, PhD</creatorcontrib><creatorcontrib>Bidstrup, Benjamin P., FRACS</creatorcontrib><creatorcontrib>Diqer, Al-Mutazz A., FRACs</creatorcontrib><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>Heart, lung &amp; circulation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alizzi, Ali M., MD</au><au>Summers, Phillip, PhD</au><au>Boon, Virginia H., BPharm (Hons)</au><au>Tantiongco, John-Paul, BMBS</au><au>Thompson, Teresa, BN</au><au>Leslie, Belinda J., BVSc</au><au>Williams, David, FRCPath</au><au>Steele, Mike, PhD</au><au>Bidstrup, Benjamin P., FRACS</au><au>Diqer, Al-Mutazz A., FRACs</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of Post-surgical Pericardial Adhesions Using a Pig Model</atitle><jtitle>Heart, lung &amp; circulation</jtitle><addtitle>Heart Lung Circ</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>21</volume><issue>1</issue><spage>22</spage><epage>29</epage><pages>22-29</pages><issn>1443-9506</issn><eissn>1444-2892</eissn><abstract>Background Post-surgical pericardial adhesions pose an increased risk of complications during redo sternotomies. Adhesive tissue formation is a normal response to tissue injury and involves complex patho-physiological processes including the actions of prostaglandins to cause plasma leakage and fibrin formation. The purpose of this study was to assess the ability of two non-steroidal anti-inflammatory agents (Indomethacin and Rofecoxib) and a barrier (Coseal, a polyethylene glycol) to limit adhesion formation following cardiac surgery in a pig model. Methods Forty-four piglets were allocated equally to four treatment groups: Group 1: Control, Group 2: intramuscular Indomethacin, Group 3: oral Rofecoxib and Group 4: Coseal sprayed on the heart. A full median sternotomy was performed on each animal and the heart exposed. Adhesions were induced by rubbing tissues with gauze, applying sutures and leaving blood in the pericardial sac before chest closure. Plasma inflammatory markers including prostaglandin E2 and thromboxane B2 were measured preoperatively and on Days 2, 5 and 10 after surgery. Eight animals from each group were slaughtered after 12 weeks and 3 after 25 weeks. Adhesions were assessed macroscopically and microscopically. Results Compared to the Control group, the extent of adhesions was significantly less in all other groups whilst adhesion density was least in the Indomethacin and Coseal groups. Indomethacin and less so Rofecoxib, inhibited the synthesis of prostaglandin E2 and thromboxane B2 but there were no significant changes in other inflammatory markers. Conclusions We conclude that systemic Indomethacin, and locally applied Coseal are suitable methods to markedly reduce pericardial and retrosternal adhesions.</abstract><cop>Australia</cop><pub>Elsevier B.V</pub><pmid>22078313</pmid><doi>10.1016/j.hlc.2011.10.002</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Adhesions
Animal model
Animals
Biological Availability
Biomarkers
Cardiovascular
Cyclooxygenase 2 Inhibitors - administration & dosage
Cyclooxygenase 2 Inhibitors - pharmacokinetics
Dinoprostone - blood
Disease Models, Animal
Drug Monitoring
Indomethacin - administration & dosage
Indomethacin - pharmacokinetics
Inflammation
Inflammation - blood
Lactones - administration & dosage
Lactones - pharmacokinetics
Pericardium
Pericardium - drug effects
Pericardium - pathology
Perioperative Period - methods
Polyethylene Glycols - administration & dosage
Polyethylene Glycols - pharmacokinetics
Postoperative Complications - blood
Postoperative Complications - etiology
Postoperative Complications - prevention & control
Prostaglandins
Sternotomy - adverse effects
Sternotomy - methods
Sulfones - administration & dosage
Sulfones - pharmacokinetics
Surface-Active Agents - administration & dosage
Surface-Active Agents - pharmacokinetics
Swine
Thromboxane B2 - blood
Tissue Adhesions - blood
Tissue Adhesions - etiology
Tissue Adhesions - pathology
Tissue Adhesions - prevention & control
Treatment Outcome
title Reduction of Post-surgical Pericardial Adhesions Using a Pig Model
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