Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine
Identifieur interne : 001319 ( Istex/Corpus ); précédent : 001318; suivant : 001320Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine
Auteurs : Seiji Kawasaki ; Nobutaka Umekita ; Tomoe Beppu ; Tatsuo Wada ; Yuichi Sugiyama ; Tatsuji Iga ; Manabu HananoSource :
- Toxicology and Applied Pharmacology [ 0041-008X ] ; 1984.
Abstract
Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p < 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.
Url:
DOI: 10.1016/0041-008X(84)90213-8
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Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Wada, Tatsuo" sort="Wada, Tatsuo" uniqKey="Wada T" first="Tatsuo" last="Wada">Tatsuo Wada</name><affiliation><mods:affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sugiyama, Yuichi" sort="Sugiyama, Yuichi" uniqKey="Sugiyama Y" first="Yuichi" last="Sugiyama">Yuichi Sugiyama</name><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iga, Tatsuji" sort="Iga, Tatsuji" uniqKey="Iga T" first="Tatsuji" last="Iga">Tatsuji Iga</name><affiliation><mods:affiliation>To whom correspondence should be addressed.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hanano, Manabu" sort="Hanano, Manabu" uniqKey="Hanano M" first="Manabu" last="Hanano">Manabu Hanano</name><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:508ABF2F938CB690FF4E51A9213E15A8A79EC772</idno><date when="1984" year="1984">1984</date><idno type="doi">10.1016/0041-008X(84)90213-8</idno><idno type="url">https://api.istex.fr/document/508ABF2F938CB690FF4E51A9213E15A8A79EC772/fulltext/pdf</idno><idno 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Beppu</name><affiliation><mods:affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Wada, Tatsuo" sort="Wada, Tatsuo" uniqKey="Wada T" first="Tatsuo" last="Wada">Tatsuo Wada</name><affiliation><mods:affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sugiyama, Yuichi" sort="Sugiyama, Yuichi" uniqKey="Sugiyama Y" first="Yuichi" last="Sugiyama">Yuichi Sugiyama</name><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iga, Tatsuji" sort="Iga, Tatsuji" uniqKey="Iga T" first="Tatsuji" last="Iga">Tatsuji Iga</name><affiliation><mods:affiliation>To whom correspondence should be addressed.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hanano, Manabu" sort="Hanano, Manabu" uniqKey="Hanano M" first="Manabu" last="Hanano">Manabu Hanano</name><affiliation><mods:affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Toxicology and Applied Pharmacology</title><title level="j" type="abbrev">YTAAP</title><idno type="ISSN">0041-008X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1984">1984</date><biblScope unit="volume">75</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="309">309</biblScope><biblScope unit="page" to="317">317</biblScope></imprint><idno type="ISSN">0041-008X</idno></series><idno type="istex">508ABF2F938CB690FF4E51A9213E15A8A79EC772</idno><idno type="DOI">10.1016/0041-008X(84)90213-8</idno><idno type="PII">0041-008X(84)90213-8</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0041-008X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p < 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Seiji Kawasaki</name><affiliations><json:string>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Nobutaka Umekita</name><affiliations><json:string>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Tomoe Beppu</name><affiliations><json:string>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Tatsuo Wada</name><affiliations><json:string>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Yuichi Sugiyama</name><affiliations><json:string>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Tatsuji Iga</name><affiliations><json:string>To whom correspondence should be addressed.</json:string><json:string>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item><json:item><name>Manabu Hanano</name><affiliations><json:string>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p > 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.</abstract><qualityIndicators><score>6.992</score><pdfVersion>1.3</pdfVersion><pdfPageSize>491.12 x 727.28 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1789</abstractCharCount><pdfWordCount>3992</pdfWordCount><pdfCharCount>26055</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>250</abstractWordCount></qualityIndicators><title>Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine</title><pii><json:string>0041-008X(84)90213-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>99</volume><pages><last>14</last><first>11</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Proc. Soc. Exp. Biol. 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In pathophysiological consequences, significant increases (p < 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.</p></abstract></profileDesc><revisionDesc><change when="1984-05-19">Registration</change><change when="1984">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YTAAP</jid><aid>84902138</aid><ce:pii>0041-008X(84)90213-8</ce:pii><ce:doi>10.1016/0041-008X(84)90213-8</ce:doi><ce:copyright type="unknown" year="1984"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This study was supported by a Grant-in-Aid for Scientific Research 57440062 provided by the Ministry of Education, Science and Culture of Japan.</ce:note-para></ce:article-footnote><ce:title>Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine</ce:title><ce:author-group><ce:author><ce:given-name>Seiji</ce:given-name><ce:surname>Kawasaki</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Nobutaka</ce:given-name><ce:surname>Umekita</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tomoe</ce:given-name><ce:surname>Beppu</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tatsuo</ce:given-name><ce:surname>Wada</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Yuichi</ce:given-name><ce:surname>Sugiyama</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tatsuji</ce:given-name><ce:surname>Iga</ce:surname><ce:cross-ref refid="COR1"><ce:sup>2</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Manabu</ce:given-name><ce:surname>Hanano</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>2</ce:label><ce:text>To whom correspondence should be addressed.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="22" month="8" year="1983"></ce:date-received><ce:date-accepted day="19" month="5" year="1984"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (<ce:italic>p</ce:italic> < 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters <ce:italic>k</ce:italic><ce:inf>12</ce:inf> (plasma to liver transfer rate constant), <ce:italic>V</ce:italic><ce:inf>2</ce:inf> (distribution volume of liver compartment), and CL<ce:inf>tot</ce:inf> (total body-plasma clearance), while a significant increase was observed in <ce:italic>k</ce:italic><ce:inf>23</ce:inf> (intrahepatic diffusion and transport rate constant); the <ce:italic>V</ce:italic><ce:inf>1</ce:inf> (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine</title></titleInfo><name type="personal"><namePart type="given">Seiji</namePart><namePart type="family">Kawasaki</namePart><affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobutaka</namePart><namePart type="family">Umekita</namePart><affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomoe</namePart><namePart type="family">Beppu</namePart><affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tatsuo</namePart><namePart type="family">Wada</namePart><affiliation>The Second Department of Surgery, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuichi</namePart><namePart type="family">Sugiyama</namePart><affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tatsuji</namePart><namePart type="family">Iga</namePart><affiliation>To whom correspondence should be addressed.</affiliation><affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Manabu</namePart><namePart type="family">Hanano</namePart><affiliation>Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1984</dateIssued><dateValid encoding="w3cdtf">1984-05-19</dateValid><copyrightDate encoding="w3cdtf">1984</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p < 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamicoxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.</abstract><note>This study was supported by a Grant-in-Aid for Scientific Research 57440062 provided by the Ministry of Education, Science and Culture of Japan.</note><relatedItem type="host"><titleInfo><title>Toxicology and Applied Pharmacology</title></titleInfo><titleInfo type="abbreviated"><title>YTAAP</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19840915</dateIssued></originInfo><identifier type="ISSN">0041-008X</identifier><identifier type="PII">S0041-008X(00)X0412-7</identifier><part><date>19840915</date><detail type="volume"><number>75</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>167</start><end>361</end></extent><extent unit="pages"><start>309</start><end>317</end></extent></part></relatedItem><identifier type="istex">508ABF2F938CB690FF4E51A9213E15A8A79EC772</identifier><identifier type="DOI">10.1016/0041-008X(84)90213-8</identifier><identifier type="PII">0041-008X(84)90213-8</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/508ABF2F938CB690FF4E51A9213E15A8A79EC772/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">PHARMACOLOGY & PHARMACY</classCode><classCode scheme="WOS">TOXICOLOGY</classCode><classCode scheme="WOS">TRANSPLANTATION</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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