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1.
ACS Appl Bio Mater ; 7(5): 2836-2850, 2024 05 20.
Article in English | MEDLINE | ID: mdl-38717017

ABSTRACT

High-altitude regions, cold deserts, permafrost regions, and the polar region have some of the severest cold conditions on earth and pose immense perils of cold injuries to exposed individuals. Accidental and unintended exposures to severe cold, either unintentionally or due to occupational risks, can greatly increase the risk of serious conditions including hypothermia, trench foot, and cold injuries like frostbite. Cold-induced vasoconstriction and intracellular/intravascular ice crystal formation lead to hypoxic conditions at the cellular level. The condition is exacerbated in individuals having inadequate and proper covering and layering, particularly when large area of the body are exposed to extremely cold environments. There is a paucity of preventive and therapeutic pharmacological modalities that have been explored for managing and treating cold injuries. Given this, an efficient modality that can potentiate the healing of frostbite was investigated by studying various complex pathophysiological changes that occur during severe cold injuries. In the current research, we report the effectiveness and healing properties of a standardized formulation, i.e., a herbosomal-loaded PEG-poloxamer topical formulation (n-HPTF), on frostbite. The intricate mechanistic pathways modulated by the novel formulation have been elucidated by studying the pathophysiological sequelae that occur following severe cold exposures leading to frostbite. The results indicate that n-HPTF ameliorates the outcome of frostbite, as it activates positive sensory nerves widely distributed in the epidermis transient receptor potential vanilloid 1 (TRPV1), significantly (p < 0.05) upregulates cytokeratin-14, promotes angiogenesis (VEGF-A), prominently represses the expression of thromboxane formation (TXA2), and significantly (p < 0.05) restores levels of enzymatic (glutathione reductase, superoxide dismutase, and catalase) and nonenzymatic antioxidants (glutathione). Additionally, n-HPTF attenuates oxidative stress and the expression of inflammatory proteins PGF-2α, NFκB-p65, TNF-α, IL-6, IL-1ß, malondialdehyde (MDA), advanced oxidative protein products (AOPP), and protein carbonylation (PCO). Masson's Trichrome staining showed that n-HPTF stimulates cellular proliferation, and increases collagen fiber deposition, which significantly (p < 0.05) promotes the healing of frostbitten tissue, as compared to control. We conclude that protection against severe cold injuries by n-HPTF is mediated via modulation of pathways involving TRPV1, VEGF-A, TXA2, redox homeostasis, and inflammatory cascades. The study is likely to have widespread implications for the prophylaxis and management of moderate-to-severe frostbite conditions.


Subject(s)
Homeostasis , Poloxamer , Polyethylene Glycols , TRPV Cation Channels , Vascular Endothelial Growth Factor A , Vascular Endothelial Growth Factor A/metabolism , TRPV Cation Channels/metabolism , Animals , Poloxamer/chemistry , Poloxamer/pharmacology , Polyethylene Glycols/chemistry , Polyethylene Glycols/pharmacology , Homeostasis/drug effects , Oxidation-Reduction , Biocompatible Materials/chemistry , Biocompatible Materials/pharmacology , Rats , Materials Testing , Cold Injury/metabolism , Cold Injury/drug therapy , Particle Size , Inflammation/drug therapy , Inflammation/metabolism , Male , Liposomes/chemistry , Humans , Administration, Topical , Frostbite/metabolism , Frostbite/drug therapy
2.
Curr Stem Cell Res Ther ; 18(4): 528-539, 2023.
Article in English | MEDLINE | ID: mdl-35838230

ABSTRACT

BACKGROUND: Though adipose-derived stem cells (ADSCs) have potential applications for the repair and regeneration of damaged tissues, limited studies have defined the function of ADSCs on dermal fibroblasts. Our RNA-seq sequencing identified differentially expressed SOCS3 in frostbite injury. OBJECTIVE: In the current study, we aim to examine the hypothesis that extracellular vesicles derived from adipose-derived mesenchymal stem cells (ADSCs-EVs) may modulate SOCS3/TGF-ß1 signaling in wound healing of frostbite injury. METHODS: sh-SOCS3 and sh-TGF-ß1 were introduced to explore the biological role of SOCS3 in frostbite injury by detecting the proliferation and migration of human skin fibroblast (HSF) cells and the wound healing in mice. Furthermore, the extracted ADSCs-EVs were interfered with HSF cells in vitro or injected into the frostbitten mouse model in vivo. RESULTS: Upregulation of SOCS3 occurred in the skin tissues of frostbitten mice. Compared to sh-NC, the wound healing rate of sh-SOCS3 presented higher on day 7(31.34±4.35 vs 41.83±3.74, p < 0.05) and day 14 (63.42±6.01 vs 88.99±5.12, p < 0.05) after injury. Silencing SOCS3 can promote frostbite wound healing. Moreover, SOCS3 downregulated TGF-ß1 to suppress the proliferation and migration of HSF cells, thus impeding the skin wound healing. Additionally, ADSCs-EVs could enhance the proliferation and migration of HSF cells according to the results of CCK-8 assay (p < 0.05), scratch test (17.82±4.25 vs 49.78±2.54, p < 0.05) and Transwell assay (42.33±6.81 vs 91.33±7.02, p < 0.05), and regulate the expression of SOCS3/TGF-ß1. The role of ADSCs-EVs in frostbite wound healing was also confirmed in vivo. ADSCs-EVs could promote frostbite wound healing by downregulating the expression of SOCS3 and upregulating the expression of TGF-ß1 and collagen I. CONCLUSION: Collectively, ADSCs-EVs inhibit SOCS3 and facilitate the expression of TGF-ß1, which promotes the proliferation and migration of HSF cells and subsequently enhances wound healing of frostbite injury.


Subject(s)
Extracellular Vesicles , Frostbite , Mesenchymal Stem Cells , Humans , Mice , Animals , Wound Healing , Transforming Growth Factor beta1/metabolism , Mesenchymal Stem Cells/metabolism , Extracellular Vesicles/metabolism , Frostbite/metabolism , Adipose Tissue/metabolism , Suppressor of Cytokine Signaling 3 Protein/genetics , Suppressor of Cytokine Signaling 3 Protein/metabolism
3.
Biochim Biophys Acta Mol Basis Dis ; 1868(6): 166385, 2022 06 01.
Article in English | MEDLINE | ID: mdl-35292361

ABSTRACT

Frostbite occurs when the skin is exposed to localized low temperatures. The main causes of frostbite are thought to be direct cell injury due to freezing of cells and tissue ischemia due to abnormal blood circulation. However, the molecular mechanism of frostbite has not been elucidated. This study aims to explain the molecular dynamics of frostbite using a mouse frostbite model and keratinocyte cell culture. Comprehensive gene expression analysis performed on mouse skin samples revealed that ß-catenin signaling is activated by frostbite. Immunohistochemistry showed nuclear translocation of ß-catenin in the skin of frostbite model mice that was not observed in mice subjected to a mechanical skin damage model induced by tape stripping. Tissue hypoxia, as detected by pimonidazole staining, coexisted with nuclear expression of ß-catenin. In keratinocyte cell cultures, nuclear translocation of ß-catenin was induced by hypoxia, but not by low temperature. Hypoxia induced epithelial-mesenchymal transition - an important biological event in the healing process of skin - and in vitro wound-healing activity, both of which were suppressed by ß-catenin inhibition. Our results suggest that during frostbite, impaired blood flow causes hypoxia, which in turn activates ß-catenin that promotes keratinocyte motility and tissue repair.


Subject(s)
Frostbite , beta Catenin , Frostbite/metabolism , Humans , Hypoxia/metabolism , Keratinocytes/metabolism , Wound Healing/physiology , beta Catenin/metabolism
4.
Artif Cells Nanomed Biotechnol ; 49(1): 11-19, 2021 Dec.
Article in English | MEDLINE | ID: mdl-33331196

ABSTRACT

In this study, novel carbon dots (CDs) were discovered and separated from Artemisiae Argyi Folium Carbonisata (AAFC) aqueous extract. AAFC-CDs were characterised by a series of methods, mainly including electron microscopy, optical technology and X-ray photoelectron spectroscopy (XPS). Results displayed that AAFC-CDs with a quantum yield (QY) around 0.19% had a size distribution between 6.0 and 10.0 nm and possessed a nearly spherical shape, with a lattice spacing of 0.369 nm. In mice, AAFC-CDs reduced the tissue damage, ear frostbite, and body stiffness caused by cold, and provided energy by increasing the use of blood glucose. The mechanism may be by decreasing concentration of IL-1ßk, TNF-α and reducing the rise in blood glucose levels caused by frostbite. This study is the first to indicate that CDs may be the active constituent of AAFC against frostbite, suggesting their potential for clinical applications.


Subject(s)
Artemisia/chemistry , Frostbite , Plant Extracts/chemistry , Plant Leaves/chemistry , Quantum Dots , Animals , Frostbite/drug therapy , Frostbite/metabolism , Interleukin-1beta/metabolism , Male , Mice , Quantum Dots/chemistry , Quantum Dots/therapeutic use , Tumor Necrosis Factor-alpha/metabolism
5.
PLoS One ; 10(2): e0116562, 2015.
Article in English | MEDLINE | ID: mdl-25714402

ABSTRACT

Ectotherms in northern latitudes are seasonally exposed to cold temperatures. To improve survival under cold stress, they use diverse mechanisms to increase temperature resistance and prevent tissue damage. The accumulation of anti-freeze proteins that improve cold hardiness occurs in diverse species including plants, arthropods, fish, and amphibians. We previously identified an Ixodes scapularis anti-freeze glycoprotein, named IAFGP, and demonstrated its cold protective function in the natural tick host and in a transgenic Drosophila model. Here we show, in a transgenic mouse model expressing an anti-freeze glycoprotein, that IAFGP protects mammalian cells and mice from cold shock and frostbite respectively. Transgenic skin samples showed reduced cell death upon cold storage ex vivo and transgenic mice demonstrated increased resistance to frostbite injury in vivo. IAFGP actively protects mammalian tissue from freezing, suggesting its application for the prevention of frostbite, and other diseases associated with cold exposure.


Subject(s)
Antifreeze Proteins/genetics , Frostbite/genetics , Gene Expression , Animals , Antifreeze Proteins/metabolism , Cell Survival/genetics , Cold Temperature , Fibroblasts/metabolism , Frostbite/metabolism , Inflammation/genetics , Inflammation/metabolism , Mice , Mice, Transgenic
6.
Vestn Ross Akad Med Nauk ; (7-8): 5-9, 2014.
Article in Russian | MEDLINE | ID: mdl-25562998

ABSTRACT

BACKGROUND: The arrest of respiration during deep hypothermia means death, though at a low temperature the heart may rhythmically contract for 30-40 minutes more. The attempts of rewarming only shorten the time before the heart arrest. Calcium ions (Ca2+) are believed to accumulate in the nervous cells in cold. An excess of these ions inhibits the metabolism. Moreover it stimulates the cell proteases, which destroy the cell membranes. AIM: The aim of the study was to make the the attempts to develop the methods of stimulating the respiration and heart without rewarming the body. MATERIALS AND METHODS: The work was carried out on wite rats 250-320g in weight. We introduced disodium salt of ethylenediaminetetraacetic acid into the animals. The second method of blocking the mechanisms of the cold death was artificial respiration. RESULTS: Ethylenediaminetetraacetic acid reacts with calcium ions, decreases their quantity in the blood, and, consequently, in a complex manner in the cell protoplasm. Artificial respiration not only increases the flow of oxygen into an organism but also decreases the lowest temperature threshold of the cold death of an organism. CONCLUSION: A decrease in the surviving threshold by 1.5-1.8 degrees C is very important from the point of view of reanimation of an organism since to preserve life in the critical period of reanimation each 0.5 degrees C are important. Prolongation of minimal frequency of heart contractions and maintaining a minimal arterial blood pressure in an overcooled organism given the body temperature of 11-12.5 degrees C is a special problem of great interest associated with many physiological and biological parameters.


Subject(s)
Calcium/metabolism , Cardiopulmonary Resuscitation , Frostbite , Heart Arrest/prevention & control , Hypothermia/therapy , Oxygen Consumption/physiology , Animals , Cardiopulmonary Resuscitation/adverse effects , Cardiopulmonary Resuscitation/methods , Cold Temperature , Disease Models, Animal , Frostbite/etiology , Frostbite/metabolism , Frostbite/physiopathology , Heart Arrest/etiology , Heart Arrest/metabolism , Heart Arrest/physiopathology , Heart Rate , Hypothermia/complications , Hypothermia/physiopathology , Male , Rats , Respiration
7.
Burns ; 40(4): 725-30, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24268642

ABSTRACT

BACKGROUND: Until now, the exact pathophysiology of frostbite injuries is poorly understood. The aim of the study is to evaluate the perfusion changes of frostbite injuries to get a better understanding of the exact mechanism underlying the resulting tissue damage. Particular attention has been given to the differentiation of changes between the various injury depths. METHODS: Cold contact injury ranging from superficial, superficial-partial, deep-partial to full thickness were generated using seven goettingen minipigs. The perfusion dynamics were assessed before and 3 h after the injuries were inflicted using the O2C-device, which combines a laser light, to determine blood flow, and white light to determine hemoglobin oxygenation and relative amount of hemoglobin. A total of 42 cold contact injuries were inflicted and 84 measurements were carried out. RESULTS: In superficial and superficial partial injuries there was an increase in the blood flow (mean, 20 ± 2.4%, 15 ± 5.1%, respectively) and in the relative amount of hemoglobin (mean, 29 ± 9.1%, 28 ± 7.2%, respectively), whereas the hemoglobin oxygenation did not alter (mean, -0.15 ± 2.4%, -0.8 ± 3.1%, respectively). In deep partial injuries there was a decrease in the blood flow (mean range, -4 ± 2.1 to -17 ± 4.7%) and an increase in the relative amount of hemoglobin (mean range, 79 ± 17.2 to 93 ± 17.7%), whereas the hemoglobin oxygenation did not alter (mean range, -0.7 ± 3.1 to -2.9 ± 3.3%). In full thickness injuries there was a drop in the blood flow (mean range, -24 ± 7.6 to -27 ± 11.8%) and in the hemoglobin oxygenation (mean range, -16 ± 3.5 to -19 ± 2.5%) and an increase in the relative amount of hemoglobin (mean range, +126 ± 19.8 to 145 ± 10.9%). CONCLUSION: The results of this study form a more precise pattern of cold contact injury perfusion changes, which can be a valuable tool to assess the degree of cold contact injury and furthermore the efficacy of novel diagnostic aids, therapeutics and treatment modalities.


Subject(s)
Frostbite/metabolism , Microcirculation , Oxygen/metabolism , Skin/metabolism , Animals , Disease Models, Animal , Laser-Doppler Flowmetry , Skin/blood supply , Spectrophotometry , Swine , Swine, Miniature
8.
Zhonghua Shao Shang Za Zhi ; 26(3): 212-5, 2010 Jun.
Article in Chinese | MEDLINE | ID: mdl-20723424

ABSTRACT

OBJECTIVE: To study the promotion effect of stromal cell-derived factor 1 (SDF-1) on the migration of epidermal stem cells (ESC) in the healing process of frostbite-wound model ex vivo. METHODS: A three-dimensional model of full-thickness frostbite of skin was constructed (with slot-like wound) out of skin equivalent. The expression of SDF-1 in wound stroma was observed with immunohistochemistry staining on post injury days (PID) 3 and 7. The model frostbite wounds were divided into control group (treated with PBS 50 microL per wound), SDF-1 group (treated with 100 ng/mL SDF-1, 50 microL per wound), and AMD3100 group [treated with 100 ng/mL AMD3100 (50 microL per wound) for 30 minutes, and then SDF-1 50 microL was added per wound]. The redistribution of ESC around wound was observed. RESULTS: The expression of SDF-1 in wound stroma increased gradually on PID 3 and 7. Compared with those in control and AMD3100 groups, there were more ESC and epithelial cell layers, and more integrin beta(1)-positive cells appeared at the basal layer of wound in SDF-1 group, and some of the positive cells migrated upward to epidermis. CONCLUSIONS: SDF-1 contributes to wound repair through promoting ESC to migrate toward and gather around wound edge. This may be one of the mechanisms of ESC participating in wound repair.


Subject(s)
Chemokine CXCL12/metabolism , Epidermal Cells , Frostbite/therapy , Stem Cells/cytology , Wound Healing , Cell Movement , Frostbite/metabolism , Humans
9.
Bull Exp Biol Med ; 146(5): 588-90, 2008 Nov.
Article in English | MEDLINE | ID: mdl-19526098

ABSTRACT

The effect of on Changes in dielectric parameters of the skin (modulus of complex dielectric permittivity |e| and dielectric loss tangent tgd) were studied on rats with local surface contact cooling followed by treatment with various cream formulations. Addition of antioxidant superoxide dismutase (SOD) to the cream significantly prevented the shifts in these parameters, which attested to less pronounced changes in the water balance in SOD-treated skin. Application of SOD during the early terms after cooling accelerated wound healing. Histological examination performed on posttraumatic day 60 revealed better integrity of the skin structures (hair follicle, sweat and sebaceous gland), which indicates ability of SOD to prevent and ameliorate the degree of cold-induced damage in the skin.


Subject(s)
Skin/drug effects , Skin/metabolism , Superoxide Dismutase/pharmacology , Animals , Frostbite/chemically induced , Frostbite/drug therapy , Frostbite/metabolism , Male , Rats , Superoxide Dismutase/administration & dosage , Wound Healing/drug effects
10.
Int J Biol Macromol ; 41(3): 260-5, 2007 Aug 01.
Article in English | MEDLINE | ID: mdl-17420045

ABSTRACT

This study develops a hybrid numerical scheme based on a molecular dynamics (MD) algorithm and the GROMACS protein data bank to analyze the thermal bio-flow of alanine molecules in a microchannel. The numerical results show that the velocity profiles in the microchannel are highly dependent on both global effects, i.e. the effective channel width and local effects, i.e. the thermal boundary conditions. Specifically, the magnitude of the fluctuations observed in the velocity profiles increase as the channel width decreases or as the thermal boundary temperature increases. The results presented in this study provide useful information regarding suitable microchannel widths and operational temperatures for bio-chip devices and contribute a further understanding of basic human thermal bio-flow phenomena, particularly, regarding the correlation between the rate of local metabolism, burn and frostbite events, respectively.


Subject(s)
Alanine/chemistry , Microfluidic Analytical Techniques , Models, Cardiovascular , Regional Blood Flow , Alanine/metabolism , Frostbite/metabolism , Humans
11.
J Anim Sci ; 84(11): 2983-9, 2006 Nov.
Article in English | MEDLINE | ID: mdl-17032792

ABSTRACT

Myostatin is a specific negative regulator of skeletal muscle growth and is regarded as one of the most important factors for myogenesis. The aim of the current study was to analyze the developmental change in the gene expression of myostatin and an adipogenic transcription factor (peroxisome proliferator-activated receptor lambda2) in the semitendinosus muscle of Japanese Black Cattle throughout the whole life cycle. An additional aim was to compare the temporal expression patterns of myostatin and relevant myogenic regulatory factors (MRF) mRNA during muscle regeneration after frostbite injury at 16 mo of age. The developmental pattern of myostatin gene expression exhibited 2 peaks: the greatest expression occurred in utero (P <0.05) and the second greatest occurred at 16 mo of age (P <0.05). The greatest level of peroxisome proliferator-activated receptor lambda2 expression was observed at 16 mo of age (P <0.05), which paralleled myostatin expression. During frostbite-induced muscle regeneration, gene expression for myostatin and 4 MRF; i.e., Myf5, MyoD, myogenin and MRF4, showed contrasting responses. Myostatin mRNA dramatically declined by 68.1 and 82.6% at 3 and 5 d after injury (P <0.05), respectively, which paralleled its protein expression, and was restored at 10 d. In contrast, the expressions of all 4 MRF mRNA were low initially but increased by 5 d after injury (P <0.05) and then remained constant or decreased slightly. These results suggest that myostatin may play a role in muscle marbling in the fattening period by decreasing myogenesis and increasing adipogenesis, and that the interaction between myostatin and MRF genes may take place at an early stage of skeletal muscle regeneration.


Subject(s)
Cattle/growth & development , Cattle/metabolism , Gene Expression Regulation, Developmental/physiology , Muscle, Skeletal/physiology , Transforming Growth Factor beta/metabolism , Animals , Female , Frostbite/metabolism , Japan , Myostatin , Pregnancy , Regeneration/physiology , Transforming Growth Factor beta/genetics
12.
Vojnosanit Pregl ; 56(4): 359-68, 1999.
Article in Serbian | MEDLINE | ID: mdl-10528521

ABSTRACT

The authors have investigated energy status of muscle tissue of the lower legs of Wistar rats subjected to freezing, as well as the dependence of ultrastructure changes in muscle tissue mitochondria on the intensity of freezing. The animals were divided into three experimental groups: two groups were exposed to cryoinjury of different intensity, while the third was the control one. Cryoinjury was applied over an experimental after thawing were taken samples of muscle tissue for the analysis of content of energy phosphates and carbohydrates' metabolites, respectively, as well as for morphometric analysis of mitochondria volume out of frozen right and unfrozen left lower legs. Results obtained from different experimental groups were compared mutually and with control group that was not exposed to cryoinjury, respectively. It was found that the freezing in muscle tissue caused hydrops degeneration of mitochondria, depletion of energy reserves, reduction of energy status and the activation of mechanism of anaerobic metabolism. All these alterations were proportional to the intensity of freezing and considerably influenced contractility function of muscle cells, causing prolonged spasm of arterioles in thawed tissue, i.e., rigor congelationis that was primarily defined as an important factor in the pathogenesis of ischemic impairment of thawed tissues.


Subject(s)
Energy Metabolism , Frostbite/metabolism , Mitochondria, Muscle/metabolism , Muscle, Skeletal/metabolism , Animals , Frostbite/pathology , Hindlimb/injuries , Male , Mitochondria, Muscle/ultrastructure , Muscle, Skeletal/ultrastructure , Rats , Rats, Wistar
13.
Br J Plast Surg ; 51(6): 450-4, 1998 Sep.
Article in English | MEDLINE | ID: mdl-9849365

ABSTRACT

The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/ day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells -76%; neutrophils -40.4%) and increased prostaglandin I2 (PGI2) (as 6-Keto-PGF1 alpha) in the involved skin. Thromboxane A2 (TxA2) (as TxB2) was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.


Subject(s)
Fibrinolytic Agents/therapeutic use , Frostbite/drug therapy , Platelet Aggregation Inhibitors/therapeutic use , Polydeoxyribonucleotides/therapeutic use , 6-Ketoprostaglandin F1 alpha/metabolism , Animals , Female , Frostbite/metabolism , Frostbite/pathology , Leukocyte Count , Male , Mast Cells/pathology , Neutrophils/pathology , Rabbits , Skin/metabolism , Skin/pathology , Thromboxane A2/metabolism
14.
Plast Reconstr Surg ; 101(7): 1881-6, 1998 Jun.
Article in English | MEDLINE | ID: mdl-9623831

ABSTRACT

The pathophysiology of cold injury is still controversial. An inflammatory process has been implicated as the underlying mechanism and certain anti-inflammatory substances such as ibuprofen and acetylsalicylic acid have been used in the clinical treatment of frostbite injury. It has been postulated that the progressive ischemic necrosis is secondary to excessive thromboxane A2 production, which upsets the normal balance between prostacyclin (prostaglandin I2) and thromboxane A2. It was aimed to clarify the pathophysiology of cold injury in this study. Twenty-one New Zealand White rabbits, each weighing 1.2 to 2.9 kg, were divided into control (n = 10) and frostbitten (n = 11) groups the randomly. The rabbit ears in the frostbitten group were subjected to cold injury, and the levels of thromboxane A2 (as thromboxane B2) and of prostaglandin I2 (as 6-keto-prostaglandin F1alpha) and the number of inflammatory cells (polymorphonuclear leukocytes and mast cells) were measured in normal and frostbitten skin of rabbit ears. The levels of 6-keto prostaglandin F1alpha and thromboxane B2, the stable metabolites of prostaglandin I2 and thromboxane A2, respectively, were increased in a statistically significant way (p < 0.002) by frostbite injury; however, thromboxane B2 increased more than 6-keto prostaglandin F1alpha. Polymorphonuclear leukocytes and mast cells, absent in normal skin, were present in the frostbitten skin. There was a statistically significant (p < 0.01) correlation between the time a rabbit ear was maintained at below -10 degrees C and skin survival and between the weights of rabbits and skin survival (p < 0.024). All these findings suggest that inflammation is involved in frostbite injury; a decrease in prostaglandin I2/thromboxane A2 ratio could be one of the factors leading to necrosis; the bigger the animal, the better its ability to counter frostbite.


Subject(s)
Epoprostenol/metabolism , Frostbite/metabolism , Frostbite/pathology , Mast Cells/pathology , Neutrophils/pathology , Thromboxane A2/metabolism , 6-Ketoprostaglandin F1 alpha/metabolism , Animals , Rabbits , Skin/injuries , Skin/metabolism , Skin/pathology , Thromboxane B2/metabolism
15.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 13(2): 118-20, 1997 May.
Article in Chinese | MEDLINE | ID: mdl-10074227

ABSTRACT

Effect of exposure to acute hypoxia and hypoxia for 2 weeks on the skin temperature and content of glycogen of frostbitten feet in rabbits were observed. The results showed that the skin temperatures and content of glycogen were decreased in frostbite at normoxia (FN) group frostbite during acute hypoxia (FAH) group and frostbite hypoxia for 2 weeks (FH-2w) group. After treatment with warm chlorhexidine immersion the skin temperature and glycogen content in treated feet of FN and FAH group were increased, as compared with untreated feet. However, there was no difference between treated and untreated feet in FH-2w group, suggesting that there may be severe disturbance of blood circulation on frostbitten feet under this condition.


Subject(s)
Frostbite/physiopathology , Glycogen/metabolism , Hypoxia/complications , Skin Temperature , Animals , Frostbite/complications , Frostbite/metabolism , Male , Muscle, Skeletal/metabolism , Rabbits
16.
Cryobiology ; 29(6): 674-8, 1992 Dec.
Article in English | MEDLINE | ID: mdl-1478097

ABSTRACT

The aim of this study was to investigate the development of the demarcation line in the rabbit ear upon injury by experimental freezing and thawing. For this purpose the sequential changes in noradrenaline (NA) content in the tissue and nerve of the ear were determined by liquid chromatography. Frostbite was inflicted with a glass bottle filled with liquid nitrogen and specimens were taken from the injured area, the probable demarcation line area and the healthy area 1, 3, and 7 days after frostbite. Control samples were taken from the normal contralateral ear. Tissue NA levels in the injured area and the probable demarcation line area were significantly lower than those in corresponding areas of the control ear after 1 day. Day 3 NA levels in the demarcation line area were 90% higher than those on Day 1 in this area and were not significantly different from Day 3 levels in the control ear. By Day 7, NA levels in the demarcation line area were down to 70% of the Day 3 levels. NA levels in the central nerve at the probable demarcation line were much higher than those in the control ear nerve and also showed a peak on Day 3. In conclusion, the results suggest that NA is released from the adrenergic nerves and the reaction at the probable demarcation line is strongest on the third day.


Subject(s)
Ear, External/injuries , Ear, External/metabolism , Frostbite/metabolism , Norepinephrine/metabolism , Adrenergic Fibers/metabolism , Animals , Ear, External/innervation , Rabbits , Time Factors
17.
Free Radic Biol Med ; 10(1): 7-11, 1991.
Article in English | MEDLINE | ID: mdl-2050298

ABSTRACT

Frostbite is characterized by acute tissue injury induced by freezing and thawing. Initial complete ischemia is followed by reperfusion and later, tissue necrosis. These vascular events support the hypothesis that free radical-mediated reperfusion injury at thawing might contribute to tissue necrosis after frostbite in a manner similar to that seen after normothermic ischemia. To test this hypothesis, rabbit ears were frozen at -21 degrees C for 30, 60, 90, or 120 s and rewarmed at room temperature (22 degrees C). Rabbits were treated "blindly" with saline alone, highly purified, pharmaceutical grade superoxide dismutase (SOD), allopurinol, or deferoxamine. The area of ear necrosis was determined 3 weeks after frostbite by "blinded" morphometry. The administration of SOD at the time of thawing significantly improved viability in ears frozen for 60 and 90 s, but not in those frozen for 30 or 120 s. Deferoxamine also improved viability in ears frozen for 60 s. Allopurinol did not significantly affect ear survival. Electron micrographs showed the appearance of severe endothelial cell injury beginning during freezing and extending through early reperfusion. Later, neutrophil adhesion, erythrocyte aggregation, and microvascular stasis were seen. These findings suggest that free radical-mediated reperfusion injury has a role in frostbite, and quantitate the proportion of the injury that is due to this mechanism.


Subject(s)
Ear/pathology , Frostbite/metabolism , Reperfusion Injury/etiology , Allopurinol/pharmacology , Animals , Deferoxamine/pharmacology , Disease Models, Animal , Free Radicals , Freezing , Frostbite/complications , Frostbite/drug therapy , Male , Necrosis , Rabbits , Reperfusion Injury/drug therapy , Superoxide Dismutase/pharmacology
18.
Gen Pharmacol ; 20(5): 641-6, 1989.
Article in English | MEDLINE | ID: mdl-2606333

ABSTRACT

1. Thioridazine and trifluoperazine, which have been previously found in this laboratory to be the most effective calmodulin antagonists in treatment of burns, are shown here to be also effective in the treatment of frostbite. 2. Electron microscopic studies have revealed a complete reversal of both the vascular and skin tissue damage induced by frostbite. 3. The reversal of the vascular damage was also demonstrated by the ability of these compounds to abolish the increase in hemoglobin content in the skin. 4. The reversal of the skin tissue damage was also revealed by the ability of these compounds to raise the decreased ATP level and the reduced activities of 6-phosphogluconate dehydrogenase and mitochondrial and soluble hexokinase in skin, induced by frostbite, to normal control levels.


Subject(s)
Calmodulin/antagonists & inhibitors , Frostbite/drug therapy , Thioridazine/therapeutic use , Trifluoperazine/therapeutic use , Adenosine Triphosphate/metabolism , Animals , Capillaries/pathology , Frostbite/metabolism , Frostbite/pathology , Hemoglobins/metabolism , Hexokinase/metabolism , Microscopy, Electron , Mitochondria/metabolism , Rats , Skin/blood supply
20.
J Hand Surg Am ; 6(1): 43-7, 1981 Jan.
Article in English | MEDLINE | ID: mdl-7204918

ABSTRACT

Observations on early pathophysiology of burning suggests that the release of prostaglandins and thromboxanes plays a role in dermal ischemia. Because of the similarities of the early-phase frostbite wound, blister fluids were aspirated from 10 patients with frostbite, and routine biochemical analysis, immunoelectrophoresis, immunodiffusion, and evaluation of prostaglandins E2, F2 alpha, and thromboxane B2 were performed. Potassium, serum glutamic-oxaloacetic transaminase (SGOT), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) levels exceeded normal serum values. All blisters were found to have IgM, IgG, IgA, C3a, and opsonin. PgE2 was present in levels less than normal, but PgF2 alpha and TxB2 were markedly elevated. Since the vasoconstricting metabolites of arachidonic acid, PgF2 alpha and TxB2, are known to mediate dermal ischemia in burns and pedicle flaps, it is suggested they may play a role in the pathogenesis of frostbite.


Subject(s)
Blister/metabolism , Exudates and Transudates/metabolism , Frostbite/etiology , Hand Injuries/etiology , Aspartate Aminotransferases/metabolism , Aspartic Acid , Creatine , Creatine Kinase/metabolism , Frostbite/metabolism , Hand Injuries/metabolism , Humans , Immunoglobulins/metabolism , L-Lactate Dehydrogenase/metabolism , Lactates , Potassium/metabolism , Prostaglandins E/metabolism , Thromboxane B2/metabolism
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