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Burn model for in vivo investigations of microcirculatory changes.

Goertz O, Vogelpohl J, Jettkant B, Daigeler A, Steinau HU, Steinstraesser L, Langer S - Eplasty (2009)

Bottom Line: 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 nonperfused area decreased during the observed period and perfusion was almost completely due to angiogenesis at day 14.The formation of edema occurred immediately postburn and decreased during the following observation time.

View Article: PubMed Central - PubMed

Affiliation: Department of Plastic and Hand Surgery, Burn Center, BG-University Hospital Bergmannsheil, Ruhr University Bochum, Buerkle-de-la-Camp-Platz 1, Bochum 44789, Germany. ole.goertz@rub.de

ABSTRACT

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 degrees 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.

No MeSH data available.


Related in: MedlinePlus

The FITC-dextran–stained ear with the burned area directly postburn in a 52-fold magnification and 1, 2, 3, 4, and 6 minutes postburn. The coagulated, nonperfused tissue appears as a dark circle in the middle of a bright surrounding, where the plasma marker FITC-dextran leaked out of the vessels into the surrounding tissue.
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Figure 3: The FITC-dextran–stained ear with the burned area directly postburn in a 52-fold magnification and 1, 2, 3, 4, and 6 minutes postburn. The coagulated, nonperfused tissue appears as a dark circle in the middle of a bright surrounding, where the plasma marker FITC-dextran leaked out of the vessels into the surrounding tissue.

Mentions: The NPA was recorded and determined with a digital planimetric mode integrated into the computer-assisted image analysis system CapImage (Figs 2, 3 and 4; Dr Zeintl, Heidelberg, Germany).


Burn model for in vivo investigations of microcirculatory changes.

Goertz O, Vogelpohl J, Jettkant B, Daigeler A, Steinau HU, Steinstraesser L, Langer S - Eplasty (2009)

The FITC-dextran–stained ear with the burned area directly postburn in a 52-fold magnification and 1, 2, 3, 4, and 6 minutes postburn. The coagulated, nonperfused tissue appears as a dark circle in the middle of a bright surrounding, where the plasma marker FITC-dextran leaked out of the vessels into the surrounding tissue.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2667331&req=5

Figure 3: The FITC-dextran–stained ear with the burned area directly postburn in a 52-fold magnification and 1, 2, 3, 4, and 6 minutes postburn. The coagulated, nonperfused tissue appears as a dark circle in the middle of a bright surrounding, where the plasma marker FITC-dextran leaked out of the vessels into the surrounding tissue.
Mentions: The NPA was recorded and determined with a digital planimetric mode integrated into the computer-assisted image analysis system CapImage (Figs 2, 3 and 4; Dr Zeintl, Heidelberg, Germany).

Bottom Line: 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 nonperfused area decreased during the observed period and perfusion was almost completely due to angiogenesis at day 14.The formation of edema occurred immediately postburn and decreased during the following observation time.

View Article: PubMed Central - PubMed

Affiliation: Department of Plastic and Hand Surgery, Burn Center, BG-University Hospital Bergmannsheil, Ruhr University Bochum, Buerkle-de-la-Camp-Platz 1, Bochum 44789, Germany. ole.goertz@rub.de

ABSTRACT

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 degrees 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.

No MeSH data available.


Related in: MedlinePlus