Effects Of Burn Trauma Research Articles

The Effect of Burn Trauma on Lipid and Glucose Metabolism: Implications for Insulin Sensitivity.

Severe burns represent a unique form of trauma in terms of the magnitude and persistence of the stress response they incur. Given advances in acute burn care in the last quarter of a century and the resultant reduction in mortality rates, even for those with massive burns, greater emphasis is now placed on understanding the metabolic stress response to severe burn trauma in order to devise strategies that promote recovery and reduce morbidity. Derangements in metabolism including protein and lipid redistribution and altered glucose handling are hallmarks of the pathophysiological response to burn trauma. In this review article, we aim to distill and discuss the c urrent literature concerning the effect of burn trauma on lipid and glucose metabolism. Furthermore, we will discuss the implications of altered lipid metabolism with regards to insulin sensitivity and glucose control, while discussing the utility of agents and strategies aimed at restoring normal lipid and glucose metabolism in burned patients.

Direct detection of blood nitric oxide reveals a burn-dependent decrease of nitric oxide in response to Pseudomonas aeruginosa infection

PurposeBurn is associated with severe immune dysfunction, including an anti-inflammatory state that occurs late after burn. While increased nitric oxide (NO) production is associated with severe infection and sepsis, the effect of burn trauma on these levels during a non-lethal infection remains unknown. We hypothesized that in a mouse model, (1) NO levels would be increased after infection without trauma and (2) burn would lead to decreased NO production even during infection. MethodsMice were infected via intra-tracheal inoculation with Pseudomonas aeruginosa 14 d following a 20% total body surface area contact burn. At 48h following infection, blood was drawn to quantify NO concentrations using a microfluidic electrochemical sensor. Significant findingsIn uninjured mice, infection caused a significant increase in blood NO levels. Increases in NO occurred in a dose-dependent response to the bacterial inoculum. Following burn, an identical infection did not elicit increases in NO. ConclusionsWhile increases in NO are expected over the course of an infection without prior trauma, burn and subsequent immune suppression decreases NO levels even in the presence of infection.

Effects of granulocyte-colony stimulating factor on wound healing in a mouse model of burn trauma.

The effects of burn trauma and granulocyte-colony stimulating factor (G-CSF) treatment on wound healing in a surgical incision model were studied. Sixty adult male mice were used in this study. Under general anesthesia hot water at 97 degrees C was applied for 3 sec to the dorsum of the mice in order to achieve 20% burn wound. After burn trauma, full thickness midline skin incision 2 cm in length was performed on the abdominal wall and then were sutured primarily with 4/0 polypropylene. In Group I only skin incision was performed, group II had skin incision and burn, in group III G-CSF (0.03 BU/30 g) was applied intraperitoneally after burn and skin incision. Breaking strength and 5-hydroxyproline (5-HP) levels of the wounds were calculated 5 and 10 days after the procedure. 5-HP levels and breaking strength values showed statistical difference between groups II-III and I-II (p<0.05). 5-HP levels were lowest in incision and burn group (41.80 microg/mg). Breaking strength levels were also lowest in the same group (0.12 kg) (p<0.05). These results suggest that third degree burn causes a significant impairment on incisional wound healing and G-CSF ameliorates this impairment.

Multivariate and vectorial analysis of pharmacological signalling: diaphragm inositol 1,4,5-triphosphate under the duress of burn trauma

Aberrant signal transduction processes within the diaphragm contribute to the weakness of this primary muscle involved in respiration. The importance of this report emphasizes how scald burn injury manifests distant systemic effects which impact on respiration. Scald burn injury from hot water is a common type of thermal injury in three specific patient groups: young children, the elderly, and the mentally and physically handicapped. Multivariate and vectorial analyses are presented within this paper with application to the effects of burn trauma on pharmacological signal transduction systems in the diaphragm. Multivariate equations showed the dependence of IP, on three to five independent variables. The independent variables included: burn size, glycerophosphate, and other polyinositols (inositol 1,4 biphosphate (I1,4P2), inositol 1 phosphate (I1P) and inositol). Graphic illustration of the equations used vectorial analysis. The multivariate analysis gives rise to a wider class of contributing factors than those observed using standard univariate relationships. This may be useful clinically in the identification of therapeutic agents for the treatment of respiratory problems in burn patients.

When Is the Burn Injury Healed?: Psychosocial Implications of Care

The psychosocial and economic effects of burn trauma are profound, not only for the patients, their families, and the burn unit staff members, but also for society as a whole. Understanding the perception of stresses experienced by patients, families, and staff is discussed, and related strategies to assist in reducing the stress are presented. A comprehensive psychosocial support system can assist the nurse in reducing the psychosocial morbidity of severe burn trauma.

Modification of calcium flux of twitch skeletal muscle in mice subjected to 20% body surface area burn.

One systemic effect of burn trauma is skeletal muscle weakness. This is the result of changes in second messenger systems involving calcium (Ca2+). Kinetic analysis of Ca2+ from cellular compartments of skeletal muscle of mice that were subjected to small burn injury (20% body surface area) was performed. Muscles of the burn group showed an increased 45Ca2+ uptake maxima compared with those of time-matched control groups. Also, 45Ca2+ efflux analysis showed a lack of differentiation between electrically stimulated tissues and nonstimulated tissues that was easily observed in time-matched control groups. This lack of differentiation indicated changes in intracellular compartmentation. It can be speculated that burn trauma may have a regulatory role in the excitation-contraction coupling mechanism by altering myoplasmic levels of Ca2+ even before skeletal muscle dysfunction occurs. These findings suggest that agents capable of controlling myoplasmic Ca2+ levels may aid in alleviating chronic skeletal muscle dysfunction in patients with burns.

Effect of burn trauma on reactivity of mouse spleen cells of different genotypes in the regional graft versus host reaction

Effect of burn trauma on reactivity of mouse spleen cells of different genotypes in the regional graft versus host reaction

Effect of burn trauma on adrenal and testicular steroid hormone production.

The effects of burn trauma in men on the production of adrenal and testicular steroids was investigated. Whereas there were significant increases in serum cortisol levels and urinary 17-hydroxycorticosteroid excretion soon after thermal injury, there were significant decreases in serum dehydroepiandrosterone sulfate, dehydroepiandrosterone, androstenedione, and testosterone concentrations during the first 4 weeks following burn trauma. Serum androstenediol and androstenediol sulfate levels also were reduced, though insignificantly, 10-23 days postburn. Serum LH levels were unchanged during the postburn interval. Since urinary 17-ketosteroid excretion was normal or below normal rather than increased, the decline in serum C19-steroid levels probably resulted from decreased glandular secretion rather than increased rates of metabolism and excretion. Low dehydroepiandrosterone sulfate and/or testosterone levels were found in some men several months after recovery from their burns. These data suggest that thermal injury leads to acute inhibition of adrenal and testicular C19-steroid secretion, but stimulation of adrenal glucocorticosteroid production, and that endocrine function in many instances is not normalized after complete healing of the burned surfaces. The mechanisms and physiological consequences of such changes in the steroid milieu of men after burn trauma are unknown.

Effect of Burn Trauma in Mice on the Generation of Cytotoxic Lymphocytes

SummaryThe mechanisms of the impaired cellular immune response after a moderately severe burn in mice was studied. T cells from spleens of burned BALB/c mice showed decreased cytotoxicity (P < 0.05) during the first 9 days postburn compared with nonburned controls. In the one-way MLC, T cells from spleens of the majority of burned BALB/c mice collected on the second, third, and fourth days postburn incubated for 6 days with irradiated spleen cells from C57BL/10J mice also had decreased cytotoxicity (P < 0.05). On the other hand, mixed populations of cells obtained from spleen or peripheral blood of burned BALB/c mice demonstrated no defect in sensitization, either in responding or stimulating abilities, in the MLC. Other experiments in which EL4 cells from burned donor C57BL mice were used to sensitize nonburned BALB/c mice showed decreased immunogenicity in recipient mice. These results indicate that the mechanism of the impaired cellular immune response after burn injury, when assayed by cytotoxicity, p...

Effect of burn trauma on glucose turnover, oxidation, and recycling in guinea pigs.

The simultaneous primed-constant infusion of [6-3H]- and [U-14C]glucose was used to determine the effect of burn injury on glucose turnover, oxidation, and recycling in guinea pigs. Eleven burned animals survived more than 72 h (survivors), whereas five died between 60 and 72 h postburn. All of the controls (n = 9) survived more than 72 h. At 48 h postburn, glucose turnover in the burned survivors was elevated 40% above that in control animals. A greater portion of the burned survivors' turnover was due to recycling and less was directed towards oxidation. The nonsurvivors had both a significantly depressed rate of appearance of glucose and an increased glucose clearance rate. Consequently, they were profoundly hypoglycemic and had a low rate of glucose oxidation. The alterations in glucose kinetics and oxidation apparent after burn did not reflect an inability of burned animals to oxidize exogenously infused glucose, however, because of 2-h infusion of 55 mumol/kg-min of unlabeled glucose doubled glucose oxidation in the burned survivors and tripled it in the nonsurvivors.

Effect of Burn Trauma on Transplanted Tumors and Chemical Carcinogenesis

Effect of Burn Trauma on Transplanted Tumors and Chemical Carcinogenesis