{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:50026"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:50026","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Etablierung eines modifizierten Adriamycin-induzierten Herzinsuffizienzmodells am Schwein","abstract":"The aim of this study was the development of a modified adriamycin induced heart failure animal model in the pig .METHODS: An intracoronary catheter was implanted directly into the left main stem in pigs and connected to a percutaneous access port that was used for repetitive Adriamycin administration (4 x 25 mg in a five day rhythm). Hemodynamic and echocardiographic variables were measured before Adriamycin administration, one week after, and 4 weeks after the last administration. Thereafter, all hearts were autopsied for detailed histologic examination. Statistical analysis was done by an analysis of variance for multiple parameters.RESULTS: All pigs had normal baseline cardiac function. Measurements after Adriamycin administration and 4 weeks later demonstrated a continued increase of the central venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and pulmonary vascular resistance, whereas cardiac output, stroke volume index, and left ventricular stroke work index decreased. These results were supported by the echocardiographic data depicting an increase of left ventricular diameters and volumes, accompanied by a decrease of intraventricular and left ventricular posterior wall thickness as well as left ventricular ejection fraction and fractional shortening. Right ventricular volumes and function did not change significantly during the trial. The histologic examination of the hearts revealed a selective toxic damage of the left ventricular myocardium with multifocal necroses and advanced tissue reorganization.CONCLUSION: This animal model creates a selective left ventricular damage that avoids ischemic damage of the myocardium. Both aspects can improve research on Adriamycin-induced cardiomyopathy, especially preventive or therapeutic strategies","abstract_html":"The aim of this study was the development of a modified adriamycin induced heart failure animal model in the pig .METHODS: An intracoronary catheter was implanted directly into the left main stem in pigs and connected to a percutaneous access port that was used for repetitive Adriamycin administration (4 x 25 mg in a five day rhythm). Hemodynamic and echocardiographic variables were measured before Adriamycin administration, one week after, and 4 weeks after the last administration. Thereafter, all hearts were autopsied for detailed histologic examination. Statistical analysis was done by an analysis of variance for multiple parameters.RESULTS: All pigs had normal baseline cardiac function. Measurements after Adriamycin administration and 4 weeks later demonstrated a continued increase of the central venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and pulmonary vascular resistance, whereas cardiac output, stroke volume index, and left ventricular stroke work index decreased. These results were supported by the echocardiographic data depicting an increase of left ventricular diameters and volumes, accompanied by a decrease of intraventricular and left ventricular posterior wall thickness as well as left ventricular ejection fraction and fractional shortening. Right ventricular volumes and function did not change significantly during the trial. The histologic examination of the hearts revealed a selective toxic damage of the left ventricular myocardium with multifocal necroses and advanced tissue reorganization.CONCLUSION: This animal model creates a selective left ventricular damage that avoids ischemic damage of the myocardium. Both aspects can improve research on Adriamycin-induced cardiomyopathy, especially preventive or therapeutic strategies","abstract_has_math":false,"creators":["Tieves, Christoph Hermann"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Christiansen, Stefan"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008","date_published":"2008","updated_at":"2026-07-30T19:40:16Z","subjects":["info:eu-repo/classification/ddc/610","Chronische Herzinsuffizienz","Herzinsuffizienz","Doxorubicin","Tiermodell","Medizin","Heart Failure","Animal model"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112590%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112590%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112590%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/50026","outbound_label":"Repository record","outbound_source":"dc:identifier"},"source_record":{"url":"https://publications.rwth-aachen.de/oai2d?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Apublications.rwth-aachen.de%3A50026","prefix":"oai_dc"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Christiansen, Stefan"]},{"key":"dc:creator","label":"Author","values":["Tieves, Christoph Hermann"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2008"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22354"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Chronische Herzinsuffizienz","Herzinsuffizienz","Doxorubicin","Tiermodell","Medizin","Heart Failure","Animal model"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/50026","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112590%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The aim of this study was the development of a modified adriamycin induced heart failure animal model in the pig .METHODS: An intracoronary catheter was implanted directly into the left main stem in pigs and connected to a percutaneous access port that was used for repetitive Adriamycin administration (4 x 25 mg in a five day rhythm). Hemodynamic and echocardiographic variables were measured before Adriamycin administration, one week after, and 4 weeks after the last administration. Thereafter, all hearts were autopsied for detailed histologic examination. Statistical analysis was done by an analysis of variance for multiple parameters.RESULTS: All pigs had normal baseline cardiac function. Measurements after Adriamycin administration and 4 weeks later demonstrated a continued increase of the central venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and pulmonary vascular resistance, whereas cardiac output, stroke volume index, and left ventricular stroke work index decreased. These results were supported by the echocardiographic data depicting an increase of left ventricular diameters and volumes, accompanied by a decrease of intraventricular and left ventricular posterior wall thickness as well as left ventricular ejection fraction and fractional shortening. Right ventricular volumes and function did not change significantly during the trial. The histologic examination of the hearts revealed a selective toxic damage of the left ventricular myocardium with multifocal necroses and advanced tissue reorganization.CONCLUSION: This animal model creates a selective left ventricular damage that avoids ischemic damage of the myocardium. Both aspects can improve research on Adriamycin-induced cardiomyopathy, especially preventive or therapeutic strategies"]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 64 S. : Ill., graph. Darst. (2008). = Aachen, Techn. Hochsch., Diss., 2008"]},{"key":"dc:title","label":"Title","values":["Etablierung eines modifizierten Adriamycin-induzierten Herzinsuffizienzmodells am Schwein"]}]}],"canonical_facts":{"dc:contributor":["Christiansen, Stefan"],"dc:coverage":["DE"],"dc:creator":["Tieves, Christoph Hermann"],"dc:date":["2008"],"dc:description":["The aim of this study was the development of a modified adriamycin induced heart failure animal model in the pig .METHODS: An intracoronary catheter was implanted directly into the left main stem in pigs and connected to a percutaneous access port that was used for repetitive Adriamycin administration (4 x 25 mg in a five day rhythm). Hemodynamic and echocardiographic variables were measured before Adriamycin administration, one week after, and 4 weeks after the last administration. Thereafter, all hearts were autopsied for detailed histologic examination. Statistical analysis was done by an analysis of variance for multiple parameters.RESULTS: All pigs had normal baseline cardiac function. Measurements after Adriamycin administration and 4 weeks later demonstrated a continued increase of the central venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and pulmonary vascular resistance, whereas cardiac output, stroke volume index, and left ventricular stroke work index decreased. These results were supported by the echocardiographic data depicting an increase of left ventricular diameters and volumes, accompanied by a decrease of intraventricular and left ventricular posterior wall thickness as well as left ventricular ejection fraction and fractional shortening. Right ventricular volumes and function did not change significantly during the trial. The histologic examination of the hearts revealed a selective toxic damage of the left ventricular myocardium with multifocal necroses and advanced tissue reorganization.CONCLUSION: This animal model creates a selective left ventricular damage that avoids ischemic damage of the myocardium. Both aspects can improve research on Adriamycin-induced cardiomyopathy, especially preventive or therapeutic strategies"],"dc:identifier":["https://publications.rwth-aachen.de/record/50026","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112590%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22354"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 64 S. : Ill., graph. Darst. (2008). = Aachen, Techn. Hochsch., Diss., 2008"],"dc:subject":["info:eu-repo/classification/ddc/610","Chronische Herzinsuffizienz","Herzinsuffizienz","Doxorubicin","Tiermodell","Medizin","Heart Failure","Animal model"],"dc:title":["Etablierung eines modifizierten Adriamycin-induzierten Herzinsuffizienzmodells am Schwein"],"dc:type":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]},"updated_at":"2026-07-30T19:40:16Z"}