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Vascular anatomy of the supraclavicular area revisited: feasibility of the free supraclavicular perforator flap. Cordova A, Pirrello R, D'Arpa S, Jeschke J, Brenner E, Moschella F. Source Cattedra di Chirurgia Plastica e Ricostruttiva, Dipartimento di Discipline Chirurgiche ed Oncologiche, Università degli Studi di Palermo, Palermo, Italy. adriana.cordova.unipa@gmail.com Abstract BACKGROUND: The supraclavicular skin has been studied extensively and used as a pedicled flap for face and neck reconstruction. Its use as a free flap has not paralleled its use as a pedicled flap. The authors performed an anatomical investigation to assess the possibility of harvesting a free supraclavicular flap with the donor-site scar lying in the supraclavicular crease. In this article, the authors present the results of their anatomical study together with the preliminary clinical applications. METHODS: Skin vascularization and feasibility of a free supraclavicular perforator flap were studied on 25 cadavers (15 fresh cadavers injected with colored latex at the Universiteé René Descartes in Paris; and 10 formalin-fixed, noninjected cadavers at the Innsbruck Medical University). The flap was used in two patients at the Plastic Surgery Department of the University of Palermo for a cutaneous facial reconstruction and intraoral reconstruction after cancer excision. RESULTS: An average of four perforators were consistently found in the supraclavicular area coming from the transverse cervical artery. Venous perforators drain into the superficial venous plexus rather than into the venae comitantes of the transverse cervical artery. Two flaps were successfully used based on these vessels. CONCLUSIONS: The vascularization of the supraclavicular skin depends on skin perforators coming from the transverse cervical artery and draining into the superficial venous plexus. Based on these vessels, a reliable free supraclavicular flap seems to be safe to harvest, with the scar hidden in the supraclavicular crease. The preliminary clinical applications of such a flap gave promising results, suggesting its potential applications.

Anatomic study on the transverse cervical vessels perforators in the lateral triangle of the neck and harvest of a new flap: the free supraclavicular transverse cervical artery perforator flap. Cordova A, D'Arpa S, Pirrello R, Brenner E, Jeschke J, Moschella F. Source Cattedra di Chirurgia Plastica e Ricostruttiva, Dipartimento di Discipline Chirurgiche ed Oncologiche, Università degli Studi di Palermo, Via del Vespro, 129-90127, Palermo, Italy. adriana.cordova.unipa@gmail.com Abstract BACKGROUND: Vessels in the supraclavicular area and their contribution to skin vascularization have always been studied for flaps planning in head and neck reconstruction and many pedicled flaps have been described based on those vessels. Little has been written instead about the vascularization of the supraclavicular skin itself for the use as a free flap. The purpose of this anatomical study was to assess the vascularization of the supraclavicular skin and the possibility of finding an adequate pedicle to harvest it as a free flap in order to close the donor site directly. METHODS: A total of 25 cadavers, 10 formalin fixed and 15 fresh, have been studied in cooperation with the Division for Clinical-Functional Anatomy, Department of Anatomy, Histology and Embryology, Innsbruck Medical University, Innsbruck, Austria and the Laboratoire d'Anatomie, Universiteé R. Descartes, Paris, France. RESULTS: The supraclavicular skin was nourished by perforators coming from the transverse cervical artery and constantly present in an average number of four. Venous drainage was accomplished through the superficial cervical vein, and not through the venae comitantes of the transverse cervical artery. CONCLUSIONS: Based on the results of this investigation, a free supraclavicular transverse cervical artery perforator (STCAP) flap seems to be feasible pedicled on perforators from the transverse cervical artery and drained by the superficial cervical vein. Due to its thickness and skin texture, it can be indicated for facial and intraoral defects, with the limitations of a relatively short pedicle. Primary closure of the donor site can be accomplished concealing the scar in the neck crease

Background The standard approach for correction of pectus carinatum deformity includes elevation of the pectoralis major and rectus abdominis muscle from the sternum and adjacent ribs. A postoperative restriction of shoulder activity for several weeks is necessary to allow stable healing of the elevated muscles. To reduce postoperative immobilization, we present a modified approach to the parasternal ribs using a pectoralis muscle split technique. Methods At each level of rib cartilage resection, the pectoralis muscle is split along the direction of its fibers instead of elevating the entire muscle as performed with the standard technique. From July 2000 to May 2007, we successfully used this technique in 33 patients with pectus carinatum deformity. Results After the muscle split approach, patients returned to full unrestricted shoulder activity as early as 3 weeks postoperatively, compared to 6 weeks in patients treated with muscle flap elevation. Postoperative pain was reduced and the patients were discharged earlier from the hospital than following the conventional approach. Conclusions The muscle split technique is a modified surgical approach to the parasternal ribs in patients with pectus carinatum deformity. It helps to maintain pectoralis muscle vascularization and function and can reduce postoperative pain, hospitalization, and rehabilitation period.

Extracorporeal shock wave therapy (ESWT) enhances tissue vascularization and neoangiogenesis. Recent animal studies showed improved soft tissue regeneration using ESWT. In most cases, deep partial-thickness burns require skin grafting; the outcome is often unsatisfactory in function and aesthetic appearance. The aim of this study was to demonstrate the effect of ESWT on skin regeneration after deep partial-thickness burns. Under general anesthesia, two standardized deep partial-thickness burns were induced on the back of 30 male Wistar rats. Immediately after the burn, ESWT was given to rats of group 1 (N=15), but not to group 2 (N=15). On days 5, 10, and 15, five rats of each group were analyzed. Reepithelialization rate was defined, perfusion units were measured, and histological analysis was performed. Digital photography was used for visual documentation. A wound score system was used. ESWT enhanced the percentage of wound closure in group 1 as compared to group 2 (P<0.05). The reepithelialization rate was improved significantly on day 15 (P<0.05). The wound score showed a significant increase in the ESWT group. ESWT improves skin regeneration of deep partial-thickness burns in rats. It may be a suitable and cost effective treatment alternative in this type of burn wounds in the future.

Occasionally during the minimally invasive repair of pectus excavatum(MIRPE), the conventional flat dissector is not rigid enough to elevate the anterior thoracic wall for bar implantation and its sharp edges may cause vessel or other tissue damage. Asa result of experiencing such complications in four cases, a new highly rigid dissector with a round cross-section was developed and its advantages are presented in a consecutive series of 21 cases.

Rationale: The neuropeptide catestatin is an endogenous nicotinic cholinergic antagonist that acts as a pleiotropic hormone. Objective: Catestatin shares several functions with angiogenic factors. We therefore reasoned that catestatin induces growth of new blood vessels. Methods and Results: Catestatin induced migration, proliferation, and antiapoptosis in endothelial cells and exerted capillary tube formation in vitro in a Matrigel assay, and such effects were mediated via G protein, mitogen-activated protein kinase, and Akt. Catestatin-induced endothelial cell functions are further mediated by basic fibroblast growth factor, as shown by blockade of effects by a neutralizing fibroblast growth factor antibody. Furthermore, catestatin released basic fibroblast growth factor from endothelial cells and stimulated fibroblast growth factor signaling. In addition to its function on endothelial cells, catestatin also exerted effects on endothelial progenitor cells and vascular smooth muscle cells. In vivo, catestatin induced angiogenesis in the mouse cornea neovascularization assay and increased blood perfusion and number of capillaries in the hindlimb ischemia model. In addition to angiogenesis, catestatin increased density of arterioles/arteries and incorporation of endothelial progenitor cells in the hindlimb ischemia model, indicating induction of arteriogenesis and postnatal vasculogenesis. Conclusion: We conclude that catestatin acts as a novel angiogenic cytokine via a basic fibroblast growth factor–dependent mechanism.

Rationale: The neuropeptide secretoneurin induces angiogenesis and postnatal vasculogenesis and is upregulated by hypoxia in skeletal muscle cells. Objective: We sought to investigate the effects of secretoneurin on therapeutic angiogenesis. Methods and Results: We generated a secretoneurin gene therapy vector. In the mouse hindlimb ischemia model secretoneurin gene therapy by intramuscular plasmid injection significantly increased secretoneurin content of injected muscles, improved functional parameters, reduced tissue necrosis, and restored blood perfusion. Increased muscular density of capillaries and arterioles/arteries demonstrates the capability of secretoneurin gene therapy to induce therapeutic angiogenesis and arteriogenesis. Furthermore, recruitment of endothelial progenitor cells was enhanced by secretoneurin gene therapy consistent with induction of postnatal vasculogenesis. Additionally, secretoneurin was able to activate nitric oxide synthase in endothelial cells and inhibition of nitric oxide inhibited secretoneurin-induced effects on chemotaxis and capillary tube formation in vitro. In vivo, secretoneurin induced nitric oxide production and inhibition of nitric oxide attenuated secretoneurin-induced effects on blood perfusion, angiogenesis, arteriogenesis, and vasculogenesis. Secretoneurin also induced upregulation of basic fibroblast growth factor and platelet-derived growth factor-B in endothelial cells. Conclusions: In summary, our data indicate that gene therapy with secretoneurin induces therapeutic angiogenesis, arteriogenesis, and vasculogenesis in the hindlimb ischemia model by a nitric oxide–dependent mechanism.

In reconstructive microsurgery, it is occasionally advantageous to use long recipient or donor vessels for optimal flap inset. These long vessels are prone to kinking or torsion along their longitudinal axis from vessel distension during blood inflow and rising blood pressure. More often than arteries, the veins can also be compressed by overlying tissue sutured under tension or by developing edema. Reanastomosis can no longer be feasible or desirable for several reasons, and the elongated vessels may have to be shifted to a curved course. To avoid detrimental kinking or torsion, fibrin glue can be administered along this new vessel course in order to ensure stabilization. In 20 such cases, we successfully avoided complications when the danger of kinking, torsion, or vein compression was evident after successful anastomosis. On the basis of this experience, we recommend the use of fibrin glue in microsurgical procedures, especially for vessels in intricate geometrical locations. © 2008 Wiley-Liss, Inc. Microsurgery, 2008.

Introduction - Secretoneurin (SN) represents a sensory, inflammatory neuropeptide which was recently demonstrated to act as an angiogenic and vasculogenic cytokine in vitro and in vivo. The present study was conducted to test the hypothesis that SN may be implicated in reparative angiogenesis. Furthermore, we challenged the healing potential of SN applied as a newly generated SN gene therapy vector in the setting of limb ischemia. Methods and Results - We cloned the human SN coding sequence into the pAAV plasmid containing a cytomegalovirus enhancer/promoter sequence. Bioactivity of recombinant SN was shown by proliferative and chemotactic activity on endothelial cells in vitro. Unilateral limb ischemia was induced in C57/bl mice by femoral artery resection. By Real Time PCR, Western Blotting, SN-specific RIA and Immunhistochemistry, we documented that SN is up-regulated in ischemic muscles. Next, we tested whether SN gene therapy may exert curative effects in this ischemia model. Injection of the SN plasmid into ischemic adductor muscles increased capillary (0.67 vs. 0.35, n = 24, p = 0.02) and arteriole (0.16 vs. 0.8, n = 24, p = 0.04) density, reduced endothelial cell apoptosis, and accelerated perfusion recovery as shown by Laser Doppler Perfusion Index (LDPI ratio ischemic/control leg after 28 days of ischemia 1.1 vs. 0.7, n = 24, p < 0.01) in comparson to pAAV-GFP (green-fluorescence protein) treated mice. Furthermore, SN gene therapy significantly reduced toe necrosis of ischemic limbs compared to control animals (26% vs. 50%, n = 24, p < 0.05). In bone marrow transplantation models, increased vascularity of ischemic hind-limbs after SN gene therapy was shown to be mediated, at least in part, by enhanced recruitment of bone marrow-derived endothelial progenitor cells. Conclusions -These results suggest that the novel angiogenic cytokine Secretoneurin is up-regulated by ischemia in skeletal muscle cells. Furthermore, results from gene therapy in this ischemia model suggest that Secretoneurin represent a promising new substance for therapeutic angiogenesis.

Expression of angiogenic cytokines like vascular endothelial growth factor is enhanced by hypoxia. We tested the hypothesis that decreased oxygen levels up-regulate the angiogenic factor secretoneurin. In vivo, muscle cells of mouse ischemic hind limbs showed increased secretoneurin expression, and inhibition of secretoneurin by a neutralizing antibody impaired the angiogenic response in this ischemia model. In a mouse soft tissue model of hypoxia, secretoneurin was increased in subcutaneous muscle fibers. In vitro, secretoneurin mRNA and protein were up-regulated in L6 myoblast cells after exposure to low oxygen levels. The hypoxia-dependent regulation of secretoneurin was tissue specific and was not observed in endothelial cells, vascular smooth muscle cells, or AtT20 pituitary tumor cells. The hypoxia-dependent induction of secretoneurin in L6 myoblasts is regulated by hypoxia-inducible factor-1alpha, since inhibition of this factor using si-RNA inhibited up-regulation of secretoneurin. Induction of secretoneurin by hypoxia was dependent on basic fibroblast growth factor in vivo and in vitro, and inhibition of this regulation by heparinase suggests an involvement of low-affinity basic fibroblast growth factor binding sites. In summary, our data show that the angiogenic cytokine secretoneurin is up-regulated by hypoxia in muscle cells by hypoxia-inducible factor-1alpha- and basic fibroblast growth factor-dependent mechanisms.