Enhancement Of Skin Flap Survival Research Articles

Photobiomodulation with polychromatic light increases zone 4 survival of transverse rectus abdominis musculocutaneous flap.

The aim of this study was to evaluate the effect of relatively novel approach of application of polychromatic light waves on flap survival of experimental musculocutaneous flap model and to investigate efficacy of this modality as a delay procedure to increase vascularization of zone 4 of transverse rectus abdominis musculocutaneous (TRAM) flap. Twenty-one Wistar rats were randomized and divided into 3 experimental groups (n = 7 each). In group 1 (control group), after being raised, the TRAM flap was sutured back to its bed without any further intervention. In group 2 (delay group), photobiomodulation (PBM) was applied for 7 days as a delay procedure, before elevation of the flap. In group 3 (PBM group), the TRAM flap was elevated, and PBM was administered immediately after the flap was sutured back to its bed for therapeutic purpose. PBM was applied in 48 hours interval from 10 cm. distance to the whole abdominal wall both in groups 2 and 3 for one week. After 7 days of postoperative follow-up, as the demarcation of necrosis of the skin paddle was obvious, skin flap survival was further evaluated by macroscopic, histological and microangiographic analysis. The mean percentage of skin flap necrosis was 56.17 ± 23.68 for group 1, 30.92 ± 17.46 for group 2 and 22.73 ± 12.98 for group 3 PBM receiving groups 2 and 3 revealed less necrosis when compared to control group and this difference was statistically significant. Vascularization in zone 4 of PBM applied groups 2 and 3 was higher compared to group 1 (P = 0.001). Acute inflammation in zone 4 of group 1 was significantly higher compared to groups 2 and 3 (P = 0.025). Similarly, evaluation of zone 1 of the flaps reveled more inflammation and less vascularization among the samples of the control group (P = 0.006 and P = 0.007, respectively). Comparison of PBM receiving two groups did not demonstrate further difference in means of vascularization and inflammation density (P = 0.259). Application of PBM in polychromatic fashion enhances skin flap survival in experimental TRAM flap model both on preoperative basis as a delay procedure or as a therapeutic approach. Lasers Surg. 51:538-549, 2019. © 2019 Wiley Periodicals, Inc.

Adipose mesenchymal stem cell-derived exosomes stimulated by hydrogen peroxide enhanced skin flap recovery in ischemia-reperfusion injury

BackgroundMesenchymal stem cell (MSC)-derived exosomes have been recognized as new candidates for the treatment of ischemic disease or injury and may be an alternative treatment for cell therapy. This aim of the study was to evaluate whether exosomes derived from adipose mesenchymal stem cell (ADSC) can protect the skin flap during ischemia-reperfusion (I/R) injury and induce neovascularization. MethodsTo investigate the effects of exosomes in the I/R injury of flap transplantation in vivo, flaps were subjected to 6 h of ischemia by ligating the left superficial inferior epigastric vessels (SIEA) followed by blood perfusion. Exosomes derived from normal ADSC (ADSC-exos) and exosomes derived from ADSC preconditioned with H2O2 (H2O2-ADSC-exos) were injected into the flaps. Then, the blood perfusion unit (BPU) of the flaps was measured by Laser Doppler Perfusion Imaging (LDPI) and microvessel density was determined by the endothelial with cell marker CD31 with Immunohistochemistry (IHC) staining. Inflammatory cell infiltration of the skin flap and apoptosis were detected by hematoxylin & eosin staining (H&E) and the TdT-mediated biotinylated dUTP nick end-labeling (TUNEL) technique. ResultsIn vivo, exosomes significantly increased flap survival and capillary density compared to I/R on postoperative day 5, and decreased the inflammatory reaction and apoptosis in the skin flap (P < 0.05). Furthermore, H2O2-ADSC-exos had better outcomes compared to normal exosomes (P < 0.05). ADSC-exos could significantly increase human umbilical vein endothelial cell (HUVEC) proliferation (P < 0.05), but no statistic difference was found in exosomes derived from different microenvironments (P > 0.05). HUVEC co-cultured with H2O2-ADSC-exos increased the migration ratio and generated more cord-like structures compared to ADSC-exos and the control group (P < 0.05). ConclusionADSC-exos can enhance skin flap survival, promote neovascularization and alleviate the inflammation reaction and apoptosis in the skin flap after I/R injury. The use of a specific microenvironment for in vitro stem cell culture, such as one containing a low concentration of H2O2, will facilitate the development of customized exosomes for cell-free therapeutic applications in skin flap transplantation.

The optimal timing of adipose derived stem cells injection to improve skin flap survival in a rat model

Background Skin flap surgery is a cornerstone in plastic surgery. However, flaps may encounter postoperative partial or complete necrosis. Different modalities have been used to enhance skin flap survival. Adipose-derived stem cells (ASCs) can promote angiogenesis and improve skin flap survival. We aimed to investigate the appropriate timing of ASC administration to get the maximal angiogenic effect and better skin flap survival in rat model.

An experimental study of the effect of pre-operative administration of cilostazol on random skin flap survival in rats: double blinded randomized controlled trial.

BackgroundInsufficient arterial blood flow is the one cause of flap necrosis. Cilostazol is an inhibitor of phosphodiesterase III and increases cyclic AMP level in vascular smooth muscle cell causing vasodilation. Therefore, effect of cilostazol is expected to improve the viability of the flap.MethodsDouble blinded randomized controlled trial was conducted. The study was to compare the survival of dorsal rat flaps between preoperative cilostazol supplemented diet and regular diet. The flap survival area was measured using PixArea Image software on post operative day 1,3,5 and 7. Fluorescein injection was performed to evaluate the exactly area of flap survival on postoperative day 7 and morphology of arterioles and venules were examined by histopathologic examination.ResultsA statistical significance was found in the percentage of area of flap survival between cilostazol supplemented diet and control group on postoperative day 3, 5 and 7 (p < 0.05). Fluorescein injection showed the higher area of flap survival in cilostazol group than the control group (p < 0.05). Histopathologic examination showed dilation of vessels in the cilostazol group.ConclusionPreoperative cilostazol in rats can enhance skin flap survival.Electronic supplementary materialThe online version of this article (doi:10.1186/s13022-015-0011-4) contains supplementary material, which is available to authorized users.

Gene therapy using hepatocyte growth factor expressing adenovirus improves skin flap survival in a rat model.

Hepatocyte growth factor (HGF) is a potent angiogenic factor that can stimulate the production of blood vessels in ischemic tissue. We investigated whether gene therapy using HGF-expressing adenovirus could enhance skin flap survival. Sprague-Dawley rats were randomly divided into three groups. Rats were subdermally injected with HGF-expressing adenovirus (HGF virus group), recombinant HGF (rhHGF group), or phosphate buffered saline (PBS group) 2 days before and immediately after 3 × 9 cm caudal flap elevation. The survival area of the skin flap, the ratio of blood flow, CD31-positive vessels and, VEGF expression were examined. Skin flap viability was significantly increased in the HGF virus group compared to the rhHGF and PBS groups (71.4% ± 5.9%, 63.8%± 6.4%, and 39.2% ± 13.0%, respectively) (P = 0.025). Furthermore, the blood flow ratio was significantly increased in the HGF virus group. In the HGF virus group, the number of CD31-positive vessels and vascular endothelial growth factor (VEGF) expression were significantly increased. Gene therapy using HGF-expressing adenovirus increase VEGF expression, the number of viable capillaries, and blood flow to the flap, thereby improving skin flap survival.

Adipose Derived Stem Cells Protect Skin Flaps Against Ischemia-Reperfusion Injury

Advances in the treatment of ischemia- reperfusion injury have created an opportunity for plastic surgeons to apply these treatments to flaps and implanted tissues. We examined the capability of adipose derived stem cells (ADSCs) to protect tissue against IRI using an extended inferior epigastric artery skin flap as a flap ischemia- reperfusion injury (IRI) model. ADSCs were isolated from Lewis rats and cultured in vitro. Twenty- four rats were randomly divided into three groups. Group I was the sham group and did not undergo ischemic insult; rather, the flap was raised and immediately sutured back (non-ischemic control group). Group II (ischemia control) and group III (ADSCs treatment) underwent 3 h of ischemic insult. During reperfusion group III was treated by intravenous application of ADSCs and group II was left untreated. Five days postoperatively, flap survival and perfusion were assessed. Microvessel density was visualized by immunohistochemistry and semi- quantitative real-time polymerase chain reaction addressed differential gene expression. Treatment with ADSCs significantly increased flap survival (p<0.001) and flap perfusion (p<0.001) when compared to the control group II. Microvessel- density in ADSCs treated group was not significantly increased in any group. No significant differences showed the comparison of the experimental group III and the sham operated control group I. ADSCs treatment (Group III) was accompanied by a significantly enhanced expression of pro-angiogenic and pro-inflammatory genes. Overall, our study demonstrates that ADSCs treatment significantly enhances skin flap survival in the aftermath of ischemia to an extent that almost equals surgical results without ischemia. This effect is accompanied with a pronounced and significant angiogenic response and an improved blood perfusion.

Fibrin-Embedded Adipose Derived Stem Cells Enhance Skin Flap Survival

Surgical skin flaps are frequently used procedures in plastic and reconstructive surgery to cover acquired or congenital defects. Either partial or total skin flap loss is a common complication, as survival of the skin flaps is determined by tissue ischemia because of insufficient vascularity. To address this issue, a number of strategies have been described to enhance blood supply and to increase skin flap survival [1–3]. Among these, stem cell-based therapies play an increasing role, due to their capacity to self-renew and differentiate into a variety of specific cell lines. Especially adipose -derived stem cells (ADSCs)—therapies have raised tremendous interest in the field of soft tissue reconstruction as they offer distinct advantages over bone marrow-derived stem cells [4]. ADSCs can be easily harvested in a minimal invasive procedure, found in abundant quantities and have the ability to differentiate into osteoblasts, chondrocytes and adipocytes in controllable and reproducible manner [5–7]. With regard to plastic and reconstructive surgery perspectives, ADSCstherapy has recently been demonstrated to improve skin flap survival [8–14]. Further investigations documented a positive effect of rescuing ischemic skin flaps by increasing tissue perfusion, a significant rise of growth factors such as vascular endothelial growth factor (VEGF) as well as fibroblast growth factor (FGF) after ADSCtherapy in rodent model [8, 10–13]. However, in all these studies ADSCs were injected into the subcutaneous tissue which may result in an uncertain distribution of the ADSCs. Furthermore the purity of the applied stem cells was not clearly analyzed. In light of these recent results this study was designed to firstly isolate and cultivate rat adipose derived stem cells and secondly determine the potential of locally applied fibrinembedded ADSCs to enhance skin flap survival in an animal epigastric skin flap model.

Augmentation of rat skin flap viability by relaxin‐expressing adenovirus

Relaxin (RLX) has multiple vascular actions, including vasodilation and angiogenesis, which occur via induction of vascular endothelial growth factor (VEGF) expression. We generated a RLX-expressing (dE1-RGD/lacZ/RLX) adenovirus and investigated whether it enhances skin flap survival. Thirty Sprague-Dawley rats were divided into three groups: RLX-expressing adenovirus group, control virus group, and phosphate-buffered saline (PBS) group. Two days before surgery and immediately after flap elevation, the caudally based flap that was 3 × 9 cm in size was subdermally injected with the dE1-RGD/lacZ/RLX virus (10⁷ PFU), dE1-RGD/lacZ virus (10⁷ PFU), or PBS. The surviving area of the flap and the amount of blood flow were measured. On postoperative day 10, CD31-positive vessels and VEGF protein expression were examined. We observed a significant increase in the survival area of the flap in the RLX group. Doppler measurement also showed significantly increased blood flow immediately after the operation and on postoperative days 7 and 10. CD31-positive vessels and VEGF protein expression were significantly greater in the RLX group. Thus, administration of RLX-expressing adenovirus into elevated skin flaps increased VEGF expression, the number of capillaries, and blood flow to the flap, thereby improving skin flap survival.

Dimethyloxalylglycine Stabilizes HIF-1α in Cultured Human Endothelial Cells and Increases Random-Pattern Skin Flap Survival In Vivo

The goal of this study was to evaluate in vitro and in vivo the effects of up-regulation of the proangiogenic hypoxia inducible factor (HIF)-1α induced by dimethyloxalylglycine on endothelial cell cultures and on skin flap survival. Human umbilical vein endothelial cell cultures were exposed to hypoxic conditions, to dimethyloxalylglycine, and to cobalt chloride for up to 24 hours. Expression of HIF-1α and vascular endothelial growth factor (VEGF) in cell culture media was analyzed. In vivo, 20 male Wistar rats were assigned randomly to either the treatment group (dimethyloxalylglycine intraperitoneal injection, n = 10) or the control group (saline intraperitoneal injection, n = 10). A dorsal skin flap was raised in all animals and sutured back into place. Flap survival was evaluated on postoperative day 7 by laser Doppler and digital planimetry. In vitro treatment of human umbilical vein endothelial cells during a 24-hour period showed a significant elevation of VEGF expression with dimethyloxalylglycine exposure (92 ± 35 pg/mg total cellular protein) or hypoxia exposure (88 ± 21 pg/mg total cellular protein) compared with controls (23 ± 10 pg/mg total cellular protein) (p < 0.05 for both). In vivo experiments showed a significant decrease of flap necrosis in the treatment group animals versus controls (35.95 ± 5.03 percent versus 44.42 ± 5.18 percent, p < 0.05). The laser Doppler evaluation revealed significantly increased blood flow in the proximal two-thirds of the flap in the treatment group compared with the control group (p < 0.05). Dimethyloxalylglycine treatment significantly increases VEGF and HIF-1α expression in endothelial cell cultures and enhances skin flap survival in vivo in a rat model.

Preoperative shock wave treatment enhances ischemic tissue survival, blood flow and angiogenesis in a rat skin flap model

Introduction Extracorporeal shock wave treatment (ESWT) has recently been shown to enhance skin flap survival. However, the bio-mechanisms operating during preoperative ESWT remain unclear. The aim of our study was to investigate whether preoperative ESWT can improve blood flow in ischemic skin flaps and to elucidate its possible mechanisms. Methods 14 male-rats were randomized into two groups and an oversized ventral random-pattern flap was raised. Experimental group received extracorporeal shock-wave treatment (ESWT) with an energy of 500 mJ/mm 2 seven days prior to total flap elevation, while control group received no treatment prior to total flap elevation. Seven days postoperatively, surviving flap area, perfused flap area, microvessel density and VEGF concentration were measured. Results Surviving flap area (59.43 ± 14.72 % to 42.71 ± 10.75 %, p = 0.026), perfused flap area (62.00 ± 8.58 % to 45.14 ± 10.50 %, p = 0.007), microvessel density (18.13 ± 5.11 to 11.09 ± 1.12, p = 0.016) and VEGF to total protein ratio (0.2107 ± 0.0935 to 0.0123 ± 0.0069, p = 0.008) were significantly elevated in the ESWT group. Conclusion Preoperative ESWT can improve skin flap survival through enhanced topical blood perfusion and neovascularization via elevation of angio-active factors.

Preoperative Shock Wave Therapy Reduces Ischemic Necrosis in an Epigastric Skin Flap Model

Extracorporeal shock wave therapy (ESWT) has recently been demonstrated to improve skin flap survival. In all these studies EWST was applied immediately after the surgical intervention. Thus, the purpose of this study was to determine the preoperative effect of ESWT as a noninvasive technique to precondition flap tissue in a rat epigastric skin flap model. EWST and control groups each contained 10 animals. ESWT was applied 7 days before the surgical intervention, whereas the control group received no treatment. Follow-up evaluation was performed on postoperative day 5. The mean area of flap necrosis, expressed as a percentage of the total flap area, was calculated. A significant reduction of the average flap necrosis area was observed in the ESWT group (27.2% +/- 9.6%) compared with the control group (46.1% +/- 7.9% (P < 0.05). In summary, this study indicates that preoperative ESWT may enhance skin flap survival in a rodent model.

Fibrin‐embedded administration of VEGF plasmid enhances skin flap survival

The aim of the present study was to experimentally evaluate whether topical fibrin-mediated administration of a vascular endothelial growth factor (VEGF)-A plasmid to the wound bed can protect skin flaps from necrosis. A plasmid expression vector containing the VEGF-A cDNA was constructed. The plasmid was then administered to the wound bed of rat abdominal skin flaps in a fibrin sealant. The percentage of viable, ischemic and necrotic tissue was assessed postoperatively as a baseline and after 3 and 7 days using digital surface area morphometry. Laser Doppler imaging of the flaps and VEGF-A Western blot analysis of flap tissue were performed to assess angiogenesis and VEGF-A tissue levels. Flaps treated with VEGF plasmids in the presence of uptake enhancing Lipofectamine transfection reagent increased flap survival 7 days postoperatively significantly associated with markedly elevated tissue perfusion and enhanced tissue VEGF-A protein expression. Our results indicate that topical fibrin-mediated administration of a VEGF-A plasmid may serve as an alternative to previous strategies in treating ischemic skin flaps. The suggested therapeutic approach is easily applicable and inexpensive in preparation. Thus, this protocol may also enhance wound healing in posttrauma skin lacerations or in skin grafts.

Enhancing skin flap survival by a cell-permeable wild-type survivin

Skin grafts, including skin flaps, are widely used in plastic and reconstructive surgery to cover wounds and tissue defects resulting from mechanic or burn injury. Ischemic necrosis is the main complication in skin graft surgery due to inefficient revascularization. Though the surgical delay procedure has been proved to be the only effective technique to prevent skin flap ischemic necrosis by mechanism of inducing adaption to hypoxia, but it is time consuming, costly, and having high risk of infection due to repeated surgery. Recent research demonstrated that, in addition to protecting cells against apoptosis, the expression of survivin correlates with intratumoral microvessel density in several different types of tumors and survivin could upregulate several proangiogenic factors, including VEGF, Egr-1 and Siah-1. Moreover, Survivin DeltaEx3, one of the survivin alternative splice variants, is necessary for activating the small GTPase Rac1 during endothelial tube formation and required for in vivo endothelial cell invasion. Therefore, we postulate that intracellular delivery of survivin or Survivin DeltaEx3 by fusion with protein transduction domain would enhance skin flap survival through accelerating revascularization by both inhibiting the apoptosis of microvascular endothelial cells and promoting skin flap angiogenesis. If the hypothesis was proved to be practical, the fusion proteins would be widely used in plastic and reconstructive surgery to prevent skin flap from ischemic necrosis in the future.

Efficacy of Combination Gene Therapy with Multiple Growth Factor cDNAs to Enhance Skin Flap Survival in a Rat Model

The objective of this study was to investigate the efficacy of combination gene therapy with multiple angiogenic growth factor cDNAs to enhance survival of ischemic skin flaps in a rat model. Sixty Sprague-Dawley rats were divided into six groups. Varying combinations of VEGF165, PDGF-B, and bFGF-plasmids were injected to prefabricate the flaps. Random skin flaps were raised on the dorsal aspect of rats following prefabrication with growth factor cDNAs. Flap viability was determined by measurement of percentage area of survival. The efficacy of gene therapy was evaluated by flap survival and neovascularization of representative histologic sections stained immunohistologically. The VEGF165 plus bFGF cDNAs enhanced the viability of the flap and neovascularization most effectively; the flap survival area was 64.3 +/- 8.7% after transfer of these two growth factor genes. Addition of PDGF-B cDNA is deleterious to the effects of combined VEGF165 and bFGF, leading to a significant decrease in flap viability (44.9 +/- 2.7%). Viability of the flaps with combined VEGF165 and bFGF cDNA transfer was significantly greater than that of the flaps with VEGF165 transfer alone (57.6 +/- 5.2%) or sham plasmid control (52.3 +/- 5.0%). Combined transfer of VEGF165 and bFGF cDNA is the most effective combination of multiple growth factor genes to improve flap viability in this model. Simultaneous transfer of three growth factor genes (VEGF165, PDGF-B, and bFGF) is deleterious to flap survival, at least for the ratio of lipofectin:transgene employed.

Dual Synergistic Effect: The Effect of Dexamethasone Plus Carnitine on Skin Flap Survival

Dexamethasone has well-known useful effects in dealing with the progression of necrosis. Carnitine is an endogenous cofactor, for having a regulatory action on the energy flow from different oxidative sources. The aim of this study was to determine whether combined local dexamethasone and systemic carnitine administration would result in an additive enhancement of skin flap survival in the rat model. A rectangular (3 cm x 11 cm) dorsal random skin flap was elevated on the rats and then sutured back into its original site with separate sutures. Overall, 40 rats were allocated randomly into 4 groups: Group 1 (control group, n = 10), group 2 (Dexamethasone group, n = 10, 2.5 mg/kg), group 3 (carnitine group, n = 10, 100 mg/kg), group 4 (dexamethasone plus carnitine group, n = 10).The mean flap survival area was 57.50 +/- 5.2% (mean survival area +/- SD) in control group (group 1), 71.5 +/- 4.8% in the dexamethasone group (group 2), 73.0 +/- 5.5% in the carnitine group (group 3), 85.30 +/- 6.1% in the dexamethasone plus carnitine group (group 4). In conclusion, based on the findings of this experimental study, the synergistic effect of carnitine and dexamethasone on skin flap viability is determined.

Local rh‐VEGF administration enhances skin flap survival more than other types of rh‐VEGF administration: a clinical, morphological and immunohistochemical study

The aim of the present study was to evaluate experimentally whether administration of recombinant (rh) vascular endothelial growth factor (VEGF) can protect skin flaps from necrosis and to study the optimum mode of rh-VEGF administration. We used rats to study the effects of local or systemic administration of rh-VEGF on skin flap during surgery; we also tested preoperative systemic administration of rh-VEGF to assess whether it may prepare the tissue to respond to the hypoxic injury better than previously tested methods. The animals were 30 male Sprague-Dawley rats. Group I rats received multiple systemic injections of rh-VEGF in the tail artery prior to flap dissection. Group II rats were injected with rh-VEGF in the clamped left epigastric artery during flap dissection; in this group, the left flaps thus received rh-VEGF locally (via incubation for 10 min during hypoxia) and the right flaps systemically, after blood flow restoration. Group III received saline solution instead of VEGF in the same way as group II. Skin samples from the distal portion of the flaps were collected on day 7 for morphological and immunohistochemical analysis. The flaps exhibiting the least necrosis were those treated with local rh-VEGF, followed by those treated with systemic rh-VEGF. The flaps that received rh-VEGF locally showed a strong VEGF expression on keratinocytes and endothelial cells, the greatest amount of mature and newly formed vessels and strong survivin expression in endothelial cells. Local rh-VEGF administration should thus be considered as an effective therapeutic option to enhance the survival of a tissue at risk for perfusion.

Propofol improves skin flap survival in a rat model: correlating reduction in flap-induced neutrophil activity.

Accumulation of neutrophils in a random pattern skin flap has been demonstrated to contribute to the necrosis of distal flap tissue. This study proposes that administration of propofol anesthesia can effectively reduce neutrophil activity and enhance skin flap survival. The study was a randomized controlled trial using male Sprague-Dawley rats as subjects. For flap survival studies, a 3- by 12-cm, dorsal, cranial-based, random pattern skin flap was elevated and reapproximated. Flaps were examined for viability 10 days postsurgery. To assess neutrophil activity, flap biopsies were taken 12, 24, or 48 hours postsurgery from distal, middle, and proximal flap regions, and myeloperoxidase enzyme content was analyzed. Animals were randomly assigned to 1 of 4 groups: group 1, ketamine anesthesia (controls); group 2, propofol anesthesia; group 3, ketamine anesthesia plus 10% lipid emulsion (propofol vehicle); group 4, ketamine anesthesia without flap elevation (nonoperated controls for myeloperoxidase study). Flap survival was significantly improved in the propofol group compared with both the ketamine and vehicle control groups (P <0.01). Increased flap viability was correlated with a reduction in myeloperoxidase content in the propofol group compared with control operated animals, with minor variations observed in the different flap regions and time points tested. This study indicates that the use of propofol can potentially improve skin flap survival. The beneficial effects may be attributed to a reduction in neutrophil activity within the flap.

Extracorporal shock wave may enhance skin flap survival in an animal model

Several methods have been used in an attempt to increase blood supply and tissue perfusion in ischemic tissues. The authors investigated the effect of extracorporal shock wave (ESW) treatment on compromised skin flaps. For this purpose, the epigastric skin flap model in rats, based solely on the right inferior epigastric vessels was used. Twenty male Sprague–Dawley rats were divided into two groups (ESW-group, Control group) of 10 rats each. The ESW-group was administered 2500 impulses at 0.15 mJ/mm 2 immediately after surgery, whereas, the control group received no treatment. Flap viability was evaluated on day 7 after the operation. Standardised digital pictures of the flaps were taken and transferred to the computer, and necrotic zones relative to total flap surface area were measured and expressed as percentages. Overall, there was a significant reduction in the surface area of the necrotic zones of the flaps in the ESW group compared to the control group (ESW group: 2.2±1.9% versus control: 17.4±4.4% ( p<0.01)). In this study, the authors demonstrated that treatment with ESW enhanced epigastric skin flap survival, as confirmed by the significant reduction of necrotic flap zones. ESW treatment seems to represent a feasible and cost effective method to improve blood supply in ischemic tissue.

Dual Preconditioning: Effects of Pharmacological Plus Ischemic Preconditioning on Skin Flap Survival

To enhance skin flap viability, pharmacological and ischemic preconditioning methods were investigated intensively. This study was designed to determine whether combined local dexamethasone administration and pedicle clamping would result in an additive enhancement of skin flap survival in the rat model. Twenty-eight male Sprague-Dawley rats were included in dexamethasone injection, clamping, clamping plus dexamethasone injection, and control groups. A rectangular random skin flap (3 x 11 cm) was outlined as bipedicled on the back of the animals. The dexamethasone or saline injection points in the flap were standardized. In the dexamethasone injection group, after raising the flaps, a total of 2.5 mg/kg dexamethasone was injected into the flaps. In the ischemic preconditioning group, 1 hour after saline injection, the cranial pedicle was clamped for 20 minutes and then 40 minutes reperfusion was performed. The clamping-plus-dexamethasone injection group was the same as the clamping group except dexamethasone was injected instead of the saline. In the control group, saline was injected instead of dexamethasone. Regardless of the group, all flaps were cut at the cranial side at the end of the 2 hours and were sutured back. On day 7, the surviving area was significantly greater in all experimental groups compared with the control group (p<0.05). Furthermore, the clamping-plus-dexamethasone group demonstrated the highest flap viability.

Effect of omental lipid fraction on enhancement of skin flap survival.

The effect of an omental lipid fraction on the rate of skin flap survival in the back of the rat was assessed by planimetric and histological examination. Compared with the control group, those rats treated with the omental lipid fraction showed significant improvement of the flap survival area. On histological examination, the flap instilled with the omental lipid fraction showed vasodilatation and neovascularization between the flap and the bed. A topical application of the omental lipid fraction enhanced the skin flap survival area, and showed vasodilatation in the flap and neovascularization between the skin flap and the recipient bed.