Impact of basic fibroblast growth factor (bFGF) on wound healing in chronically ischemic tissue.
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Biomedical subjects
M Kamler
Publications and source records attributed to M Kamler.
The hairless mouse ear: an in vivo model for studying wound neovascularization.
Microvascular ingrowth into damaged tissue is an essential component of the normal healing process. In fact, wound therapy is often aimed at promoting neovascularization. However, little is known about the mechanisms that regulate microvascular ingrowth into a healing wound. This limited knowledge is largely due to the lack of adequate models in which microvascular ingrowth can be quantitatively analyzed throughout the healing process. To address this deficiency, we developed a model in which a wound was created on the ear of the hairless mouse-a well established model for directly viewing and measuring skin microcirculation. While the animals were under ketamine and xylazine anesthesia, 2.25 mm diameter full-thickness wounds were created on the dorsum of hairless mouse ears down to but not including the cartilage (0.125 mm depth). With the use of video microscopy and computer-assisted digitized planimetry, the precise epithelial and neovascular wound edge was viewed and measured regularly throughout healing. Therefore, this model can provide objective data on wound epithelialization and neovascularization throughout healing. This model was used to examine the effect of topical wound agents on epithelialization and neovascularization. Differential effects by these anti-microbial agents on these two processes were observed, which suggests clinical implications for their use.
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Ketanserin accelerates wound epithelialization and neovascularization.
We investigated the acute effects of topical ketanserin, a 5-HT(2) (serotonin) receptor blocker, on wound epithelialization and vascularization with the use of the hairless mouse ear model. Varying concentrations of Ketanserin (0%, 0.2%, 2.0%, 20% weight/volume) were administered to standardized full-thickness skin wounds on the dorsum of the hairless mouse ear immediately after surgery and daily thereafter. With the use of video microscopy and computer-assisted planimetry, vascularization and epithelialization were traced every third day until the wounds were fully healed. Arteriole diameters at selected sites near the skin wound were measured before wound creation and after wounding. It was concluded that topically administered ketanserin significantly accelerates both the vascular (p < 0.001 at 2% and 20% concentrations) and epithelial (p < 0.001 at 20% concentration) rates of wound healing in full-thickness nonpathologic skin wounds. Vasodilation of terminal arterioles was not a major response to Ketanserin. Faster epithelialization was possibly due to direct effect of ketanserin on epithelial cells.
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Impact of ischemia on tissue oxygenation and wound healing: intravital microscopic studies on the hairless mouse ear model.
To determine the effect of ischemia on tissue oxygenation and the healing of experimental wounds, chronic ischemia was induced in the ears of hairless mice by ligating 2 of the 3 main nutritional arteries. Tissue ischemia was verified by measurement of transcutaneous pO2 (tcpO2) prior to and on days 3, 6, 9, 12 and 15 after vessel ligation. TcpO2 values decreased from 24 to 6 mm Hg at day 2 after ligation, and slowly recovered to 12 mm Hg at day 12 after vessel ligation. In animals treated with the vasoactive drug buflomedil (3 mg/kg BW i.v., startling 2 days after vessel ligation) tcpO2 values were significantly higher on days 6 and 9 when compared to saline-treated control animals. In order to find out whether the enhanced tissue oxygenation resulted in enhancement of healing of wounds, we created circular wounds (diameter = 2.5 mm, depth 0.1 mm) on ischemic ears 2 days after vessel ligation. The wound surface area was measured by means of intravital fluorescence microscopy and digital planimetry at 3-day intervals until the time of wound closure. These experiments were performed on buflomedil-treated and control animals receiving equivalent amounts of saline. The reduction of wound surface area was accelerated and wound closure time was reduced from 15 days in control animals to 12 days in buflomedil-treated animals (p < 0.01). Functional capillary density as well as the microhemodynamic parameters microvessel diameter and red blood cell velocity were not different between buflomedil-treated and control animals.
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