• Title/Summary/Keyword: Skin burn injury

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Effects of Lepidii Semen on Acute Edematous Lung Injury Induced by Skin Burn

  • Myoung-Je Cho;Hyun Gug Cho
    • Biomedical Science Letters
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    • v.9 no.1
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    • pp.37-42
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    • 2003
  • The present study was conducted to determine whether administration of heat extract of Lepidii Semen has an inhibitory effect on neutrophil-derived oxidative injury following dermal scald burn in rats. Acute lung injury was induced by scald burn (15% of TBSA) in rats. To identify acute edematous lung injury, protein concentrations and numbers of polymorphonuclear leukocytes were measured in bronchoalveolar lavage (BAL) at 5 h after skin burn. In addition, the level of lung KC (neutrophil chemoattractant cytokine) and activity of lung myeloperoxidase (MPO) were measured, and histopathological changes were observed as well. Lung weight and concentration of BAL protein, the index of lung injury, were clearly increased at 5 h postburn compared with those of sham-operated group. Administration of heat extract of Lepidii Semen after scald burn inhibited the production of KC in lung tissue and decreased the activity of lung MPO related to infiltration of neutrophils. In histopathological changes in lung tissue, infiltration of inflammatory cells and pulmonary edema induced by skin burn were decreased by administration of heat extract of Lepidii Semen after scald burn. These results suggest that Lepidii Semen may be an effective medical stuff for acute lung injury induced by skin burn.

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Skin Spread of Rhubarb Mixed with Olibanum and Myrrha Decreases KC Level in Skin and Serum Following Scald Burn Injury

  • Park, Jin-Yong;Kang, Byung-Soo
    • Biomedical Science Letters
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    • v.7 no.3
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    • pp.145-149
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    • 2001
  • The present study was conducted to determine whether local production of neutrophil chemoattractant cytokines preceded the influx of neutrophils 1311owing dermal scald burn injury. In order to inhibit the influx of neutrophils, we induced scald burn injury on dorsal skin of rats (TBSA 15%) and spread Rhubarb (R. undulatum L.) and complex (Rhubarb+Olibanum+Myrrha) on scald skin in rats. 1. Levels of dermal KC, the indicator of skin iuflammation, caused by burn gradually increased 5 hours, 24 hours (p<0.001) and 72 hours (p<0.001) after the burn occurred. After 24 hours it occurs, KC in skin was decreased by both skin spread of Rhubarb (p<0.05) and complex (p<0.05) compared to scald bum group. After 72 hours, KC by skin sp.end of Rhubarb and complex was significantly decreased (p<0.01), and the inhibition effect of KC production by complex is higher than by Rhubarb. 2. KC content in serum was increased (p<0.01) at 24 hours after burn injury and comes down back to the normal level after 72 hours. At 24 hours postbunt both Rhubarb (p<0.05) and complex (p<0.01) skin spread decreased KC in serum. The inhibition effect of KC production by complex skin spread group is higher than by Rhubarb skin spread group. The data suggest that the KC production effects by Rhubarb skin spread group and complex skin spread group are high. Especially the endurance of the effect by complex skin spread group was longer than by Rhubarb skin spread group. The inhibition effect of KC production by complex skin spread group increases more than by Rhubarb skin spread group as time passes.

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A study on Histologically Change of the Skin and Liver in Skin Burn (피부화상에 의한 피부 및 간의 조직학적 변화에 관한 연구)

  • Kim, Han-Soo;Kim, Sang-Soo;Kim, Yong-Kwon
    • Journal of Korean Physical Therapy Science
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    • v.8 no.1
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    • pp.923-934
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    • 2001
  • In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald bum, biochemical assay and morphological changes in skin tissue, serum and liver tissue were examined. The effects of bum injury on the levels of glutathione, lipid peroxide and on the activities of oxygen free radical generating and scavenging enzymes have been determined in association with observing of histologic and ultrastructural changes, measuring the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. The activity of xanthine oxidase, an enzyme of oxygen free radical generating system. was elevated (p<0.01) in serum, but not in skin and in liver tissue. Futhermore, thermal injury decreased not only the protein concentration in plasma but also the number of leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

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Numerical Study on Skin Burn Injury due to Flash Flame Exposure (돌발화염으로 인한 화상예측에 관한 수치해석적 연구)

  • Lee, Jun-Kyoung;Bang, Chang-Hoon
    • Fire Science and Engineering
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    • v.26 no.5
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    • pp.13-20
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    • 2012
  • Many fire-fighters suffer from the burn injuries, and the severe burns are the most catastrophic injury a person can survive, resulting in pain, emotional stress, and tremendous economic costs. It is important to understand the physiology of burns for prevention from skin burns and a successful treatment of a burn patient. But a few researches have been presented because the complex physical phenomena of our inside body like non-linearity characteristics of human skin make them difficult. Thus in this study, thermal analyses of biological tissues exposed to a flash fire causing severe tissue damage were studied by using a finite difference method based on the Pennes bio-heat equation. The several previous models for skin thermo-physical properties were summarized, and the calculated values with those models of tissue injury were compared with the results obtained by the previous experiment for low heat flux conditions. The skin models with good agreement could be found. Also, the skin burn injury prediction results with the best model for high heat flux conditions by flash flame were suggested.

Acceleration of Wound Healing on Scald Burn Skin Using Irradiation of TDP and Skin Spread of Myrrha

  • Cho Hyun Gug;Kim Keum-Suk;Lee Jong-wook
    • Biomedical Science Letters
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    • v.11 no.2
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    • pp.243-248
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    • 2005
  • The present study was conducted to determine whether skin spread of Myrrha and Tending Diancibo Pu (TDP) irradiation have a remarkable effect on the cell regeneration as well as wound healing following dermal scald burn injury. Burn injury was induced on dorsal surface $(TBSA\;15\~20\%)$ by scald burn in rats. Postburn concentration of serum protein was significantly decreased compared with sham-treated, double treatment with Myrrha and TDP was significantly increased the protein concentration compared with that of burn control. The content of keratinocyte growth factor (KGF) at 48 h is higher than that of at 24 h, and double treatment with Myrrha and TDP was the most effective to increase the production of KGF in all experimental groups. Morphologically, epithelial regeneration and dermal collagen synthesis by fibroblasts were accelerated in Myrrha and TDP treated group compared with bum control at same time postburn. At 48 h after burn, all dermal connective tissues are recovered to new collagen fibers in case of Myrrha and TDP double treated group. The data suggest that double treatment with skin spread of Myrrha and TDP radiation have a remarkable effect of to accelerate cell regeneration and wound healing in case of scald burn skin.

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Effect of Mori Cortex in the Cardiac Injury Induced by Skin Burn

  • Moon, Hye-Jung;Cho, Hyun-Gug;Park, Won-Hark
    • Biomedical Science Letters
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    • v.10 no.2
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    • pp.107-113
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    • 2004
  • This study was conducted to investigate an effect of Mori Cortex in the cardiac injury following dermal scald burn in rats. Sprague-Dawley rats were induced scald bum (15% of total body surface area). Heart was removed at 5 h postburn and examined with biochemical assay, ultrastructural observations and stereological analysis. The activity of serum aspartate aminotransferase and creatinine was increased at 5 h postburn compared with them of control. Administration of heat extracts of Mori Cortex after scald burn inhibited the production of KC (neutrophil chemoattractant cytokine) and increased the activity of protein kinase C (PKC) in heart tissue. The activity of myeloperoxidase (MPO) in heart tissue was decreased both at 5 h postburn and in case of Mori Cortex administration after scald burn. Ultrastructurally, many contraction bands and separation of intercalated disk induced by scald burn were decreased by administration of heat extracts of Mori Cortex. In stereological analysis, administration of Mori Cortex after scald burn resulted the volume densities of myofibril and mitochondria were increased compared with them of burn control. These data suggest that Mori Cortex may be a useful stuff to the range of available treatments for cardiac injury induced by skin burn.

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Effect of Skin Burn on the Activities of Free Radical Generating and Scavenging Enzymes in Rat Liver (피부화상이 간의 유해산소 생성계 및 해독계 효소 활성에 미치는 영향)

  • Park, Rae-Jun;Kim, Han-Soo;Bae, Ju-Han;Lee, Hyun-Kee;Choi, Jae-Won;Lee, Dong-Ho
    • The Journal of Korean Physical Therapy
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    • v.14 no.1
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    • pp.63-73
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    • 2002
  • In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay in skin tissue, serum and liver tissue were examined. The effects of burn injury on the levels of glutathione, lipid peroxide and on the activities of oxygen of histologic and ultrasound changes, measuring. the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. Post burn 24 h, the content of glutathione was decreased (47.50%), whereas that of lipid peroxide was increased (37.01%), and the activity of superoxide dismutase was diminished (p<0.001). Thus decreasing the capacity of oxygen free radical scavenging enzymes led to oxidative injury in skin tissue. In liver tissue, at 24 h after scald burn, both the content of glutathione and the activity of catalase were markedly decreased (p<0.01, p<0.05), thus the imbalance between free radical generating and scavenging capacities has been induced.

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Allopurinol Decreases Liver Damage Induced by Dermal Scald Burn Injury (피부 화상으로 유도된 간 손상에서 Allopurinol의 효과)

  • Cho, Hyun-Gug;Yoon, Chong-Guk;Park, Won-Hark
    • Applied Microscopy
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    • v.31 no.1
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    • pp.37-47
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    • 2001
  • In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total burn surface area $20\sim25\%$) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay and morphological changes in serum and liver tissue were examined. Skin burn increased liver weight (% of body weight, p<0.05) and the activity of serum aniline amino-transferase (ALT, p<0.05), in addition, the activity of xanthine oxidase (XO), an enzyme of oxygen free radical generating system, was elevated (p<0.01) in serum, but not in skin and in liver. Postburn treatment of allopurinol intraperitoneally decreased liver weight, serum ALT activity and serum XO activity. Scald burn induced ultrastructurally swelling of endoplasmic reticulum, ribosome detachment, accumulation of lipid, dilatation of bile canaliculi and intercellular space, neutrophil infiltration, activation of Kupffer's cells and degeneration of hepatocytic microvilli. Futhermore , thermal injury decreased not only the protein concentration in plasma but also the number of intravascular leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. However allopurinol injection after burn inhibited post burn ultrastructural changes. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

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Clinical Characteristics of Thermal Injuries Following Free TRAM Flap Breast Reconstruction (확장 광배근 근피판술을 이용한 유방재건술)

  • Park, Jae Hee;Bang, Sa Ik;Kim, Suk Han;Im, So Young;Mun, Goo Hyun;Hyon, Won Sok;Oh, Kap Sung
    • Archives of Plastic Surgery
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    • v.32 no.4
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    • pp.408-415
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    • 2005
  • Following a transverse rectus abdominis musculocutaneous(TRAM) flap breast reconstruction, denervated state of the flap causes the flap skin prone to thermal injury, calling for special attention. During the last 5 years, 69 breast reconstruction with 72 free TRAM flaps, were performed. Four out of thesse 69 patients sustained burn injury. Heat sources were a warm bag(n=2), heating pad(n=1) and warming light (n=1). The thermal injuries occured from 2 days to 3 months following the reconstruction. Three patients healed with conservative treatment, but one patient required debridement and skin graft. Initially 3 out of 4 patients with the burn had shown superficial 2nd degree burn with small blebs or bullae. However all 4 patients healed with scars. Mechanism of burn injuries of the denervated flap are known to be resulting from; 1) loss of behavioral protection due to denervation of flap with flap elevation and transfer, 2) loss of autonomic thermoregulatory control with heat dissipation on skin flap vasculature contributing to susceptibility of burn injury. 3) changes of immunologic and normal inflammatory response increasing thromboxane, and a fall in substance P & NGF (nerve growth factor). Including the abdominal flap donor site, sensory recovery of the reconstructed breast varies individually from 6 month even to 5 years postoperatively. During this period, wound healing is delayed, resulting in easier scarring compared to that observed in the sensate skin. Patients should be carefully informed and warned of possible burn injuries and taught to avoid exposure to heat source at least until 3 years postoperatively.

Clinical Characteristics of Thermal Injuries Following Free TRAM Flap Breast Reconstruction (횡복직근 유리피판술로 유방재건 후 발생한 화상의 임상적 특성)

  • Lee, Paik Kwon;Bae, Joon Sung;Ahn, Sang Tae;Oh, Deuk Young;Rhie, Jong Won;Han, Ki Taik
    • Archives of Plastic Surgery
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    • v.32 no.4
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    • pp.403-407
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    • 2005
  • Following a transverse rectus abdominis musculocutaneous(TRAM) flap breast reconstruction, denervated state of the flap causes the flap skin prone to thermal injury, calling for special attention. During the last 5 years, 69 breast reconstruction with 72 free TRAM flaps, were performed. Four out of thesse 69 patients sustained burn injury. Heat sources were a warm bag(n=2), heating pad(n=1) and warming light (n=1). The thermal injuries occured from 2 days to 3 months following the reconstruction. Three patients healed with conservative treatment, but one patient required debridement and skin graft. Initially 3 out of 4 patients with the burn had shown superficial 2nd degree burn with small blebs or bullae. However all 4 patients healed with scars. Mechanism of burn injuries of the denervated flap are known to be resulting from; 1) loss of behavioral protection due to denervation of flap with flap elevation and transfer, 2) loss of autonomic thermoregulatory control with heat dissipation on skin flap vasculature contributing to susceptibility of burn injury. 3) changes of immunologic and normal inflammatory response increasing thromboxane, and a fall in substance P & NGF (nerve growth factor). Including the abdominal flap donor site, sensory recovery of the reconstructed breast varies individually from 6 month even to 5 years postoperatively. During this period, wound healing is delayed, resulting in easier scarring compared to that observed in the sensate skin. Patients should be carefully informed and warned of possible burn injuries and taught to avoid exposure to heat source at least until 3 years postoperatively.