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Burn Model for In Vivo Investigations of Microcirculatory Changes
Objective: The treatment of burns remains a challenge due to the associated high morbidity and mortality. Besides the administration of physiologic saline, local disinfection, and symptomatic medications, no causal therapy is known to reduce the tissue damage and accelerate wound healing. The aim of...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Open Science Company, LLC
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667331/ https://www.ncbi.nlm.nih.gov/pubmed/19412334 |
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author | Goertz, Ole Vogelpohl, Julian Jettkant, Birger Daigeler, Adrien Steinau, Hans Ulrich Steinstraesser, Lars Langer, Stefan |
author_facet | Goertz, Ole Vogelpohl, Julian Jettkant, Birger Daigeler, Adrien Steinau, Hans Ulrich Steinstraesser, Lars Langer, Stefan |
author_sort | Goertz, Ole |
collection | PubMed |
description | Objective: The treatment of burns remains a challenge due to the associated high morbidity and mortality. Besides the administration of physiologic saline, local disinfection, and symptomatic medications, no causal therapy is known to reduce the tissue damage and accelerate wound healing. The aim of the study was to develop a reliable burn model that allows for reproducible quantitative in vivo analysis of the microcirculation, angiogenesis, and leukocyte endothelium interaction after burn injury. Methods: Experiments were carried out on male hairless mice (n = 9). Full-thickness burns were inflicted with a hot air jet without any contact to the tissue (117 ± 2.1°C for 1 second; burn area: 1.3 mm(2)). Intravital fluorescent microscopy, in combination with FITC-dextran as plasma marker, was used to assess microcirculatory standard parameters; leukocytes were stained with rhodamine 6G. Values were obtained before, immediately after, as well as at days 1, 3, 7, and 14 postburn. Results: The nonperfused area decreased during the observed period and perfusion was almost completely due to angiogenesis at day 14. No posttraumatic expansion of the nonperfused area after 24 hours could be observed. Leukocyte endothelium interaction showed its maximum 24 hours postburn. The formation of edema occurred immediately postburn and decreased during the following observation time. Conclusion: The developed burn model allows a reproducible assessment with significant results of the microcirculation, angiogenesis, and leukocyte endothelium interaction without causing mechanical damage to the tissue; therefore, this model qualifies for the further investigations of interventional drugs to decrease the effects of burn injury. |
format | Text |
id | pubmed-2667331 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Open Science Company, LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-26673312009-05-03 Burn Model for In Vivo Investigations of Microcirculatory Changes Goertz, Ole Vogelpohl, Julian Jettkant, Birger Daigeler, Adrien Steinau, Hans Ulrich Steinstraesser, Lars Langer, Stefan Eplasty Article Objective: The treatment of burns remains a challenge due to the associated high morbidity and mortality. Besides the administration of physiologic saline, local disinfection, and symptomatic medications, no causal therapy is known to reduce the tissue damage and accelerate wound healing. The aim of the study was to develop a reliable burn model that allows for reproducible quantitative in vivo analysis of the microcirculation, angiogenesis, and leukocyte endothelium interaction after burn injury. Methods: Experiments were carried out on male hairless mice (n = 9). Full-thickness burns were inflicted with a hot air jet without any contact to the tissue (117 ± 2.1°C for 1 second; burn area: 1.3 mm(2)). Intravital fluorescent microscopy, in combination with FITC-dextran as plasma marker, was used to assess microcirculatory standard parameters; leukocytes were stained with rhodamine 6G. Values were obtained before, immediately after, as well as at days 1, 3, 7, and 14 postburn. Results: The nonperfused area decreased during the observed period and perfusion was almost completely due to angiogenesis at day 14. No posttraumatic expansion of the nonperfused area after 24 hours could be observed. Leukocyte endothelium interaction showed its maximum 24 hours postburn. The formation of edema occurred immediately postburn and decreased during the following observation time. Conclusion: The developed burn model allows a reproducible assessment with significant results of the microcirculation, angiogenesis, and leukocyte endothelium interaction without causing mechanical damage to the tissue; therefore, this model qualifies for the further investigations of interventional drugs to decrease the effects of burn injury. Open Science Company, LLC 2009-04-03 /pmc/articles/PMC2667331/ /pubmed/19412334 Text en Copyright © 2009 The Author(s) http://creativecommons.org/licenses/by/2.0/ This is an open-access article whereby the authors retain copyright of the work. The article is distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Article Goertz, Ole Vogelpohl, Julian Jettkant, Birger Daigeler, Adrien Steinau, Hans Ulrich Steinstraesser, Lars Langer, Stefan Burn Model for In Vivo Investigations of Microcirculatory Changes |
title | Burn Model for In Vivo Investigations of Microcirculatory Changes |
title_full | Burn Model for In Vivo Investigations of Microcirculatory Changes |
title_fullStr | Burn Model for In Vivo Investigations of Microcirculatory Changes |
title_full_unstemmed | Burn Model for In Vivo Investigations of Microcirculatory Changes |
title_short | Burn Model for In Vivo Investigations of Microcirculatory Changes |
title_sort | burn model for in vivo investigations of microcirculatory changes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667331/ https://www.ncbi.nlm.nih.gov/pubmed/19412334 |
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