A Histologic Perspective on Electrical and Thermal Burn-Injured Human Skin.

OBJECTIVE: To analyze specific spectroscopic (FT-Raman) and thermal (limiting oxygen index) aspects of skin samples exposed to electrical injury compared with thermal injury. METHODS: An observational case-control study was conducted at the Dr Stanislaw Sakiel Center for Burns Treatment in Siemianowice, Silesia, Poland. A scanning electron microscope was used to diagnose and illustrate the topography of skin samples from electrical and thermal burns and the morphologic effects on damaged versus undamaged skin surfaces. In particular, researchers attempted to detect spectroscopic and thermal changes at the molecular level, namely, specific biomarkers of tissue degeneration and their regeneration under the influence of the applied modifiers (antioxidants and orthosilicic acid solutions). RESULTS: Modification with L-ascorbic acid and hydrogel of orthosilicic acid caused an increase in the intensity of the amide I Raman peaks, whereas modification with sodium ascorbate and orthosilicic acid resulted in the separation of the band protein side chains (1,440-1,448 cm), which is a part of tissue regeneration. The best result was obtained when the skin was treated with 7% orthosilicic acid (limiting oxygen index, 26%). CONCLUSIONS: Antioxidant treatment may be advantageous in minimizing injury in patients with thermal burns but not always in electrical burns.

Targeted release of stromal cell-derived factor-1α by reactive oxygen species-sensitive nanoparticles results in bone marrow stromal cell chemotaxis and homing, and repair of vascular injury caused by electrical burns.

Rapid repair of vascular injury is an important prognostic factor for electrical burns. This repair is achieved mainly via stromal cell-derived factor (SDF)-1α promoting the mobilization, chemotaxis, homing, and targeted differentiation of bone marrow mesenchymal stem cells (BMSCs) into endothelial cells. Forming a concentration gradient from the site of local damage in the circulation is essential to the role of SDF-1α. In a previous study, we developed reactive oxygen species (ROS)-sensitive PPADT nanoparticles containing SDF-1α that could degrade in response to high concentration of ROS in tissue lesions, achieving the goal of targeted SDF-1α release. In the current study, a rat vascular injury model of electrical burns was used to evaluate the effects of targeted release of SDF-1α using PPADT nanoparticles on the chemotaxis of BMSCs and the repair of vascular injury. Continuous exposure to 220 V for 6 s could damage rat vascular endothelial cells, strip off the inner layer, significantly elevate the local level of ROS, and decrease the level of SDF-1α. After injection of Cy5-labeled SDF-1α-PPADT nanoparticles, the distribution of Cy5 fluorescence suggested that SDF-1α was distributed primarily at the injury site, and the local SDF-1α levels increased significantly. Seven days after injury with nanoparticles injection, aggregation of exogenous green fluorescent protein-labeled BMSCs at the injury site was observed. Ten days after injury, the endothelial cell arrangement was better organized and continuous, with relatively intact vascular morphology and more blood vessels. These results showed that SDF-1α-PPADT nanoparticles targeted the SDF-1α release at the site of injury, directing BMSC chemotaxis and homing, thereby promoting vascular repair in response to electrical burns.

LL-37-derived peptides eradicate multidrug-resistant Staphylococcus aureus from thermally wounded human skin equivalents.

Burn wound infections are often difficult to treat due to the presence of multidrug-resistant bacterial strains and biofilms. Currently, mupirocin is used to eradicate methicillin-resistant Staphylococcus aureus (MRSA) from colonized persons; however, mupirocin resistance is also emerging. Since we consider antimicrobial peptides to be promising candidates for the development of novel anti-infective agents, we studied the antibacterial activities of a set of synthetic peptides against different strains of S. aureus, including mupirocin-resistant MRSA strains. The peptides were derived from P60.4Ac, a peptide based on the human cathelicidin LL-37. The results showed that peptide 10 (P10) was the only peptide more efficient than P60.4Ac, which is better than LL-37, in killing MRSA strain LUH14616. All three peptides displayed good antibiofilm activities. However, both P10 and P60.4Ac were more efficient than LL-37 in eliminating biofilm-associated bacteria. No toxic effects of these three peptides on human epidermal models were detected, as observed morphologically and by staining for mitochondrial activity. In addition, P60.4Ac and P10, but not LL-37, eradicated MRSA LUH14616 and the mupirocin-resistant MRSA strain LUH15051 from thermally wounded human skin equivalents (HSE). Interestingly, P60.4Ac and P10, but not mupirocin, eradicated LUH15051 from the HSEs. None of the peptides affected the excretion of interleukin 8 (IL-8) by thermally wounded HSEs upon MRSA exposure. In conclusion, the synthetic peptides P60.4Ac and P10 appear to be attractive candidates for the development of novel local therapies to treat patients with burn wounds infected with multidrug-resistant bacteria.

Effects of parecoxib on the prevention of postoperative peritoneal adhesions in rats.

BACKGROUND: No systemic preventive therapy has been successful in inhibiting the development of postoperative peritoneal adhesions (PPAs). OBJECTIVE: The aim of this study was to evaluate the potential effects of 5 day administration of parecoxib, on PPA prevention and on suture or wound healing in rats. METHODS: In a model of PPAs induced by peritoneal electrical burn, 30 rats were randomized into 3 groups according to parecoxib administration route (control; intraperitoneal (IP); intramuscular (IM)). Plasma and peritoneal levels of PAI-1 and tPA were measured at T0, after 90 min of surgery (T90), and on postoperative day 10 (D10). In a cecum resection model, 20 rats were randomized into two groups (control and IP parecoxib), and abdominal wound healing and suture leakage were assessed at D10. In both models, PPAs were evaluated quantitatively and qualitatively on D10. RESULTS: Administration of parecoxib significantly decreased the quantity (p < .05) and the severity (p < .01) of PPAs in both models. In addition, parecoxib administration did not cause healing defects or infectious complications in the two models. In the peritoneal burn model, IP or IM parecoxib administration inhibited the increase of postoperative plasma and peritoneum PAI-1 levels, an increase that was observed in the control group (p < .01). No anastomosis leakage could be demonstrated in both groups in the cecum resection model. CONCLUSION: This study showed that, in these rat models, parecoxib might reduce PPA formation. Confirmation of the safety of parecoxib on intestinal anastomoses is required and should be investigated in further animal models.

Effect of lidocaine on reducing injury in a rat electrical burn model.

Electrical injuries induce progressive tissue loss. We evaluated the effect of lidocaine on tissue necrosis after electrical burn injuries. Forty-two male Wistar albino rats (250-300 g) were divided into 3 groups [Group A (n=6), control group without an electrical burn injury; and Groups B (n=18) and C (n=18), electrical burn injury groups without and with lidocaine therapy, respectively]. Three separate analyses were performed at different time points on 6 of 18 rats from Groups B and C at each time point. Electrical burns were induced by applying 220 V AC between the left upper and right lower extremities for 10 seconds. Myeloperoxidase and malondialdehyde levels were measured in skin and muscle biopsy specimens after the first hour, fresh and dry weight differences in the amputated extremities were calculated after 24 hours, and live and necrotic tissue areas were measured at 7 days after burn injury. We found that lidocaine reduced edema, the number of neutrophils, and neutrophil damage in tissues. We conclude that lidocaine decreased the amount of necrotic tissue caused by electric injury.

Burn wound angiogenesis is increased by exogenously administered recombinant leptin in rats.

BACKGROUND: Leptin is a potent direct angiogenic factor that stimulates endothelial cell migration and activation in vitro and angiogenesis in vivo. In addition, leptin has been discussed to play an important role in angiogenesis, as it promotes the formation of new blood vessels. PURPOSE: The effect of exogenously administered leptin on the healing process of a full tissue burn wound model. METHODS: Sixty-three Sprague-Dawley male rats were used. Full tissue burn wound was created by electrocautery. The width of the pin was 0.3 cm; its length was 2 cm and was used at the "cut" modulation. Rats were divided into seven groups of nine animals each. Burn wounds were injected with murine recombinant leptin and the rats were sacrificed 3, 7 and 9 days after surgery. Every group had obtained three animals for the three different days of sacrifice. Three different leptin doses of 250 pg/ml, 500 pg/ml and 1000 pg/ml were used in different animal groups (A, B and C). For every one of the three leptin doses used, another animal group was evaluated by using the combined injection of leptin and antileptin (A1, B1, and C1), in order to study the inhibitory effect to the leptin factor. Nine rats were served as controls. These were injected with 0.3 ml water for injection solution and sacrificed at the same time intervals. After sacrifice of the animals, the skin was grossly determined by its appearance, colour and texture. Full thickness burn wounds were dissected for histological examination. A qualitative analysis of angiogenesis in the burn wound was conducted following a standard hematoxylin and eosin stain. The wound tissue samples from each experimental group underwent immunohistochemical evaluation of microvessel density by endothelial cell staining with mouse anti-rat CD 34 monoclonal antibody. RESULTS: The most impressive growth of new blood vessels appeared seven and nine days after treatment with the highest leptin doses. There were no significant differences in microvessel density between the seventh and the ninth postoperative day among different groups treated with leptin. All wounds from the control group, as well as those from animal groups treated with the combined injection of leptin and antileptin did not develop any new vessels. CONCLUSION: Exogenous administration of recombinant leptin increases early tissue angiogenesis in the burn wound level of an experimental animal model.

Burn wound angiogenesis is increased by exogenously administered recombinant leptin in rats

BACKGROUND: Leptin is a potent direct angiogenic factor that stimulates endothelial cell migration and activation in vitro and angiogenesis in vivo. In addition, leptin has been discussed to play an important role in angiogenesis, as it promotes the formation of new blood vessels. PURPOSE: The effect of exogenously administered leptin on the healing process of a full tissue burn wound model. METHODS: Sixty-three Sprague-Dawley male rats were used. Full tissue burn wound was created by electrocautery. The width of the pin was 0.3 cm; its length was 2 cm and was used at the "cut" modulation. Rats were divided into seven groups of nine animals each. Burn wounds were injected with murine recombinant leptin and the rats were sacrificed 3, 7 and 9 days after surgery. Every group had obtained three animals for the three different days of sacrifice. Three different leptin doses of 250 pg/ml, 500 pg/ml and 1000 pg/ml were used in different animal groups (A, B and C). For every one of the three leptin doses used, another animal group was evaluated by using the combined injection of leptin and antileptin (A1, B1, and C1), in order to study the inhibitory effect to the leptin factor. Nine rats were served as controls. These were injected with 0.3 ml water for injection solution and sacrificed at the same time intervals. After sacrifice of the animals, the skin was grossly determined by its appearance, colour and texture. Full thickness burn wounds were dissected for histological examination. A qualitative analysis of angiogenesis in the burn wound was conducted following a standard hematoxylin and eosin stain. The wound tissue samples from each experimental group underwent immunohistochemical evaluation of microvessel density by endothelial cell staining with mouse anti-rat CD 34 monoclonal antibody. RESULTS: The most impressive growth of new blood vessels appeared seven and nine days after treatment with the highest leptin doses. There were no significant...

INTRODUÇÃO: A leptina é um potente fator angiogênico que estimula a migração e a ativação de células endoteliais in vitro e a angiogênese in vivo. Além disso, a leptina tem sido considerada importante na angiogênese pois ela promove a formação de novos vasos sanguíneos. OBJETIVO: Investigar o efeito da leptina administrada por via exógena no processo de cicatrização em um modelo experimental de queimadura. MÉTODOS: Foram utilizados sessenta e três ratos Sprague-Dawley, machos. A lesão de espessura total da queimadura foi realizada por eletrocautério. O dano tecidual foi de 0.3 cm numa extensão de 2 cm tendo sido empregada o módulo de "corte"do eletrocautéio. Os ratos foram distribuídos em sete grupos de nove animais. As lesões por queimadura receberam leptina recombinante. Os animais foram sacrificados 3, 7 e 9 dias após o ato operatório. Obteve-se três animais de cada grupo nos três períodos estipulados. Três diferentes dosagens de leptina: 250 pg/ml, 500 pg/ml e 1000 pg/ml foram aplicados nos três diferentes grupos (A, B e C). Para cada uma das três dosagens de leptina, outro grupo de animais foi avaliado pelo uso de injeção combinada de leptina e antileptina (A1, B1 e C1) no sentido de investigar o efeito inibitório do fator leptina. Nove ratos serviram de controles. Estes foram submetidos à injeção de 0.3 ml de água e sacrificados nos mesmos intervalos de tempo. Após o sacrifício dos animais, o tegumento foi avaliado por sua aparência, cor e textura. Fragmentos das feridas queimadas foram ressecadas para exame histológico. A análise qualitativa de angiogênese, na ferida queimada, seguia o padrão da coloração de hematoxilina e eosina. Cada fragmento de tecido, de cada grupo experimental, foi submetido à avaliação imunohistoquímica da densidade dos microvasos pela coloração da célula endotelial por anti-rato CD 34 anticorpo monoclonal. RESULTADOS: O desenvolvimento de novos vasos sanguíneos foi mais significativo após sete e nove dias...

[Early surgical treatment of injured persons with subfascial electric burn of extremities in combination with preparation Betadine]. / Rannee khirurgicheskoe lechenie postsradavshikh s subfastsial'nym élektroozhogom konechnostei v komplekse s preparatom Betadin.

Basing on the clinical material analysis, on bacteriological investigation data, smear-"prints", the authors recommend application of 10% solution of Betadine for sanatation of the electric wounds with subfascial structures affection, what have permitted to accelerate the wound surface clearance, to reduce exudation, to activate the primary granulation tissue development to prepare the wound for its plastic closure. Application of Betadine in conditions of aseptic inflammation had promoted the secondary necrosis occurrence in the tissue ischemia after deep burn occurrence.

[Experimental high-voltage electrical burns on limbs of rabbits].

OBJECTIVE: The study was designed to investigate the changes in some rheological parameters and ET-1 in venous blood following electrical burns. METHODS: One of the hind limbs of rabbits was subjected to 3000 V, 2.5 A charge of alternative electric current for 3 seconds. Rheological parameters such as red cell deformability (RED) and platelet aggregation rate (PAR), as well as endothelin-1 (ET-1) in venous blood drained from electrical burn wounds and contents of ATP in damaged muscle were measured at time intervals of 2 h, 24 h, 48 h and 72 h postburn. RESULTS: The changes in the parameters mentioned above were significant following electrical injury. The administration of PGE1 showed an advantageous effect in prevention of thrombosis and muscle "progressive necrosis" through improvement in RCD, reduction of PAR and the content of ET-1 in local circulation. CONCLUSION: RCD, PAR and the content of ET-1 in local circulation changed significantly following electric injury and may play an important role in the process of "progressive necrosis". The potential use of PGE1 in the treatment of electrical injury is proposed.

Genital tract burns during rollerball endometrial coagulation.

Thermal injuries occurred in three women after hysteroscopic rollerball endometrial ablation. Possible mechanisms of injury included insulation failure of the rollerball to the sheath of the resectoscope, current division with the sheath acting as an alternate return electrode, and capacitative leakage of current from the active electrode to the sheath.

A new explanation for the progressive tissue loss in electrical injuries.

A reproducible electrical injury to the hind limb was produced in rats, an injury characterized by progressive tissue necrosis. Serial histochemical examinations of cross sections with a peroxidase-antiperoxidase method revealed increased production of arachidonic acid metabolites, especially thromboxane, at distal sites near the entrance wound and in periosseous tissues more proximally. Levels of these vasoactive substances remained elevated during the time of progressive necrosis and demarcation of seemingly normal, uninjured tissue. Treatment with agents capable of blocking thromboxane production allowed tissue salvage, as evidenced by a decreased autoamputation rate and an increased total surviving length. From this study it appears that an electrical injury is thermal trauma, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged thromboxane excess, with resultant vasoconstriction and thrombosis in the microcirculation, is seen to play a key role in the progressive tissue loss characteristic of the injury. The use of antithromboxane agents may be of benefit in halting this progression and salvaging tissue in these devastating injuries.