Ultrastructural features of canine hepatic auxiliary transplant rejection
Auxiliary canine hepatic homografts were examined electron microscopically 24 hours to 17 days after transplantation. Many nonspecific changes were present. Early, the endoplasmic reticulum was dilated and the mitochondria were abnormal. After the initial postoperative period, autophagic vacuoles, s...
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Veröffentlicht in: | Experimental and molecular pathology 1967-06, Vol.6 (3), p.361-369 |
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description | Auxiliary canine hepatic homografts were examined electron microscopically 24 hours to 17 days after transplantation. Many nonspecific changes were present. Early, the endoplasmic reticulum was dilated and the mitochondria were abnormal. After the initial postoperative period, autophagic vacuoles, shedding of cytoplasm, light and dark cells, and acidophilic bodies were present and macrophages were common. Initial ischemic cell injury can be explained by vascular derangements inherent in the process of transplantation. Its persistency may result from impaired perfusion by excess mesenchymal cells in sinusoids and tissue spaces and by competition between these and hepatocytes for nutrients. An immunologic component is suggested by the presence of large mononuclear cells, with many ribosomes seen in delayed type hypersensitivity reactions. These were closely approximated to and indenting the hepatic parenchymal cells, but bridging between the mesenchymal cells or hepatocytes was not found. The similarity of the mesenchymal cells and their relation to hepatocytes in chronic active hepatitis in man supports the idea that in both transplant rejection and in the human disease an immunologic process mediated by cells adds to the destruction of hepatic tissue. |
doi_str_mv | 10.1016/0014-4800(67)90018-4 |
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Many nonspecific changes were present. Early, the endoplasmic reticulum was dilated and the mitochondria were abnormal. After the initial postoperative period, autophagic vacuoles, shedding of cytoplasm, light and dark cells, and acidophilic bodies were present and macrophages were common. Initial ischemic cell injury can be explained by vascular derangements inherent in the process of transplantation. Its persistency may result from impaired perfusion by excess mesenchymal cells in sinusoids and tissue spaces and by competition between these and hepatocytes for nutrients. An immunologic component is suggested by the presence of large mononuclear cells, with many ribosomes seen in delayed type hypersensitivity reactions. These were closely approximated to and indenting the hepatic parenchymal cells, but bridging between the mesenchymal cells or hepatocytes was not found. The similarity of the mesenchymal cells and their relation to hepatocytes in chronic active hepatitis in man supports the idea that in both transplant rejection and in the human disease an immunologic process mediated by cells adds to the destruction of hepatic tissue.</description><identifier>ISSN: 0014-4800</identifier><identifier>EISSN: 1096-0945</identifier><identifier>DOI: 10.1016/0014-4800(67)90018-4</identifier><identifier>PMID: 5339252</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Dogs ; Endoplasmic Reticulum ; Hypersensitivity, Delayed - pathology ; Ischemia ; Liver - pathology ; Liver Transplantation ; Microscopy, Electron ; Mitochondria ; Transplantation Immunology ; Transplantation, Homologous</subject><ispartof>Experimental and molecular pathology, 1967-06, Vol.6 (3), p.361-369</ispartof><rights>1967</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-6083a059008205dbf71f911c059bee6ac48cc3d9b3e4ec49531e2a2ff7b89f3b3</citedby><cites>FETCH-LOGICAL-c357t-6083a059008205dbf71f911c059bee6ac48cc3d9b3e4ec49531e2a2ff7b89f3b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0014480067900184$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/5339252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klion, Franklin M</creatorcontrib><creatorcontrib>Schaffner, Fenton</creatorcontrib><title>Ultrastructural features of canine hepatic auxiliary transplant rejection</title><title>Experimental and molecular pathology</title><addtitle>Exp Mol Pathol</addtitle><description>Auxiliary canine hepatic homografts were examined electron microscopically 24 hours to 17 days after transplantation. Many nonspecific changes were present. Early, the endoplasmic reticulum was dilated and the mitochondria were abnormal. After the initial postoperative period, autophagic vacuoles, shedding of cytoplasm, light and dark cells, and acidophilic bodies were present and macrophages were common. Initial ischemic cell injury can be explained by vascular derangements inherent in the process of transplantation. Its persistency may result from impaired perfusion by excess mesenchymal cells in sinusoids and tissue spaces and by competition between these and hepatocytes for nutrients. An immunologic component is suggested by the presence of large mononuclear cells, with many ribosomes seen in delayed type hypersensitivity reactions. These were closely approximated to and indenting the hepatic parenchymal cells, but bridging between the mesenchymal cells or hepatocytes was not found. The similarity of the mesenchymal cells and their relation to hepatocytes in chronic active hepatitis in man supports the idea that in both transplant rejection and in the human disease an immunologic process mediated by cells adds to the destruction of hepatic tissue.</description><subject>Animals</subject><subject>Dogs</subject><subject>Endoplasmic Reticulum</subject><subject>Hypersensitivity, Delayed - pathology</subject><subject>Ischemia</subject><subject>Liver - pathology</subject><subject>Liver Transplantation</subject><subject>Microscopy, Electron</subject><subject>Mitochondria</subject><subject>Transplantation Immunology</subject><subject>Transplantation, Homologous</subject><issn>0014-4800</issn><issn>1096-0945</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1967</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EKqXwByBlhWARGMfOwxskVPGoVIkNXVuOMxau0qTYDoK_x6FVl6w89tw7vnMIuaRwR4EW9wCUp7wCuCnKWxFvVcqPyJSCKFIQPD8m04PklJx5vwYAATSbkEnOmMjybEoWqzY45YMbdBicahODKhbok94kWnW2w-QDtypYnajh27ZWuZ8kWjq_bVUXEodr1MH23Tk5Mar1eLE_Z2T1_PQ-f02Xby-L-eMy1SwvQ1pAxRTkMW-VQd7UpqRGUKrjU41YKM0rrVkjaoYcNRc5o5ipzJiyroRhNZuR693cres_B_RBbqzX2MY02A9eVpwLQRmPQr4Tatd779DIrbObGF9SkCNBOeKRIx5ZlPKPoBxtV_v5Q73B5mDaI4v9h10f45JfFp302mKnsbEukpBNb___4BdwfYCv</recordid><startdate>196706</startdate><enddate>196706</enddate><creator>Klion, Franklin M</creator><creator>Schaffner, Fenton</creator><general>Elsevier Inc</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>196706</creationdate><title>Ultrastructural features of canine hepatic auxiliary transplant rejection</title><author>Klion, Franklin M ; Schaffner, Fenton</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357t-6083a059008205dbf71f911c059bee6ac48cc3d9b3e4ec49531e2a2ff7b89f3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1967</creationdate><topic>Animals</topic><topic>Dogs</topic><topic>Endoplasmic Reticulum</topic><topic>Hypersensitivity, Delayed - pathology</topic><topic>Ischemia</topic><topic>Liver - pathology</topic><topic>Liver Transplantation</topic><topic>Microscopy, Electron</topic><topic>Mitochondria</topic><topic>Transplantation Immunology</topic><topic>Transplantation, Homologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klion, Franklin M</creatorcontrib><creatorcontrib>Schaffner, Fenton</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>Experimental and molecular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klion, Franklin M</au><au>Schaffner, Fenton</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ultrastructural features of canine hepatic auxiliary transplant rejection</atitle><jtitle>Experimental and molecular pathology</jtitle><addtitle>Exp Mol Pathol</addtitle><date>1967-06</date><risdate>1967</risdate><volume>6</volume><issue>3</issue><spage>361</spage><epage>369</epage><pages>361-369</pages><issn>0014-4800</issn><eissn>1096-0945</eissn><abstract>Auxiliary canine hepatic homografts were examined electron microscopically 24 hours to 17 days after transplantation. Many nonspecific changes were present. Early, the endoplasmic reticulum was dilated and the mitochondria were abnormal. After the initial postoperative period, autophagic vacuoles, shedding of cytoplasm, light and dark cells, and acidophilic bodies were present and macrophages were common. Initial ischemic cell injury can be explained by vascular derangements inherent in the process of transplantation. Its persistency may result from impaired perfusion by excess mesenchymal cells in sinusoids and tissue spaces and by competition between these and hepatocytes for nutrients. An immunologic component is suggested by the presence of large mononuclear cells, with many ribosomes seen in delayed type hypersensitivity reactions. These were closely approximated to and indenting the hepatic parenchymal cells, but bridging between the mesenchymal cells or hepatocytes was not found. The similarity of the mesenchymal cells and their relation to hepatocytes in chronic active hepatitis in man supports the idea that in both transplant rejection and in the human disease an immunologic process mediated by cells adds to the destruction of hepatic tissue.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>5339252</pmid><doi>10.1016/0014-4800(67)90018-4</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Dogs Endoplasmic Reticulum Hypersensitivity, Delayed - pathology Ischemia Liver - pathology Liver Transplantation Microscopy, Electron Mitochondria Transplantation Immunology Transplantation, Homologous |
title | Ultrastructural features of canine hepatic auxiliary transplant rejection |
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