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PubMed1999

Burn injury with infection alters prostaglandin E2 synthesis and metabolism.

OBJECTIVE: The aim of this study was to examine the relationship between prostaglandin synthesis and prostaglandin degradation in a model of burn injury with infection. METHODS: Male B2D6F1 mice were assigned to control, burn (16% dorsal scald burn), or burn with infection (burn with topical application of 1,000 colony forming units of Pseudomonas aeruginosa) groups. Lung tissue was harvested at 1, 2, and 3 days after burn injury and subsequently processed for total RNA and protein. Northern and Western blot analyses were used to examine differences in cyclooxygenase 2 (COX-2) and prostaglandin 15-OH dehydrogenase (PGDH) protein and mRNA expression. Total RNA was probed with the riboprobe for murine PGDH and COX-2 and the 100,000g protein fraction was immunoblotted by using an rabbit anti-murine PGDH and anti-murine COX-2 antibody. RESULTS: COX-2 expression was elevated in the burn with infection animals on day 1 and day 2 after burn injury. At these time points in the burn + infection group, PGDH was significantly depressed. Burn injury increased COX-2 expression on day 1, but by day 2, COX-2 expression had decreased to control values. A corresponding increase in PGDH expression was observed on day 2 in the burned mice. The mRNA expression of COX-2 was followed by a similar increase in COX-2 protein expression at all time points in the injured animals. This was not the case with PGDH expression. On day 1, PGDH mRNA expression was depressed in the burn with infection mice with no change in PGDH protein expression. This finding indicates that PGDH is subject to regulation at both the transcriptional and posttranscriptional levels. CONCLUSION: Burn wound infection depressed both PGDH mRNA and protein expression and increased COX-2 mRNA and protein expression. Therefore, increases in circulating prostaglandin E2 levels during septic injury are derived from alterations in synthesis and degradation of prostaglandin E2.

Animals↗
PubMed2000

Effect of nitric oxide synthase inhibitor on experimentally induced burn wounds.

BACKGROUND: Nitric oxide (NO) may have an important role in the healing of burn wounds. This study investigated the effect of NO on experimentally induced burn wounds by preventing NO synthesis. METHODS: A total of 40 mice weighing 25 to 30 g were used in this study. The shaved skin on the back of the mice was immersed in 100 degrees C water for 10 seconds to achieve a partial-thickness scald burn. The mice were divided into two groups of 20. In group I (control group), 17.5 mg/kg of serum physiologic (placebo) was injected intraperitoneally two times a day for 15 days. In group II (study group), 17.5 mg/kg of aminoguanidine (NO synthase inhibitor) was injected intraperitoneally two times a day for 15 days. On day 15 of the burn, the animals were killed and the burn areas were investigated histologically. Histologic changes such as epithelial proliferation, abscess, collagen, and granulation tissue were evaluated. RESULTS: Epithelial proliferation, formation of collagen, and granulation tissue with rich capillaries observed in the control group were statically significantly higher than those observed in the study group (z = -2.022, p < 0.05; z = -2.02, p < 0.05; and z = -2.022, p < 0.05; respectively). CONCLUSION: We concluded that healing of the burn wound is delayed by preventing NO synthesis.

Animals↗
PubMed2000

Resuscitation of severe thermal injury with hypertonic saline dextran: effects on peripheral and visceral edema in sheep.

BACKGROUND: Edema of tissue not directly injured by heat is a common complication after resuscitation of burn shock. Hypertonic 7.5% NaCl 6% dextran (HSD) infusion reduces early fluid requirements in burn shock, but the effects of HSD on peripheral and visceral tissue edema are not well-defined. METHODS: We measured the microcirculatory absorptive pressures of burned and nonburned skin and tissue water content of skin and other tissues in anesthetized sheep after 70% to 85% total body surface area scald and resuscitation. Fluid infusion was initiated 30 minutes after injury using 10 mL/kg HSD (n = 11) or lactated Ringer's (LR) (n = 12), with infusion rates titrated to restore and maintain preburn oxygen delivery (DO2). Thereafter, both groups received LR infusions as needed to maintain DO2 until the study's end at 8 hours. Colloid osmotic pressure was measured in plasma, and combined interstitial colloid osmotic and hydrostatic pressures were measured in skin. RESULTS: Both treatments successfully restored DO2, but fluid requirements were less with the HSD group than with the LR group (43+/-19 mL/kg vs. 194+/-38 mL/kg, respectively, p < 0.05). The peripheral and visceral tissue water contents at 8 hours postinjury until the end of the study in both burn groups were significantly higher than in nonburn controls. However, HSD-treated sheep had significantly less water content in the colon (less 28%), liver (less 9%), pancreas (less 55%), skeletal muscle (less 21%), and nonburned skin (less 12%) compared with LR-treated sheep (p < 0.05 for each). HSD-treated sheep maintained significantly higher (3 to 5 mm Hg) plasma colloid osmotic pressure than LR-treated sheep. CONCLUSION: There were no observed differences in edema in burn skin between the two treatment groups. The early volume-sparing effect of HSD and reduction in tissue edema are likely attributed to an increased extracellular osmolarity and a better maintenance of the plasma oncotic pressure.

Animals↗
PubMed2001

Antioxidant vitamin therapy alters burn trauma-mediated cardiac NF-kappaB activation and cardiomyocyte cytokine secretion.

BACKGROUND: This study examined the effects of antioxidant vitamins A, C, and E on nuclear transcription factor-kappa B (NF-kappaB) nuclear translocation, on secretion of inflammatory cytokines by cardiac myocytes, and on cardiac function after major burn trauma. METHODS: Adult rats were divided into four experimental groups: group I, shams; group II, shams given oral antioxidant vitamins (vitamin C, 38 mg/kg; vitamin E, 27 U/kg; vitamin A, 41 U/kg 24 hours before and immediately after burn); group III, burns (third-degree scald burn over 40% total body surface area) given lactated Ringer's solution (4 mL/kg/% burn); and group IV, burns given lactated Ringer's solution plus vitamins as described above. Hearts were collected 4, 8, 12, and 24 hours after burn to assay for NF-kappaB nuclear translocation, and hearts collected 24 hours after burn were examined for cardiac contractile function or tumor necrosis factor-alpha secretion by cardiomyocytes. RESULTS: Compared with shams, left ventricular pressure was lower in burns given lactated Ringer's solution (group III) (88 +/- 3 vs. 64 +/- 5 mm Hg, p < 0.01) as was +dP/dt max (2,190 +/- 30 vs. 1,321 +/- 122 mm Hg/s) and -dP/dt max (1,775 +/- 71 vs. 999 +/- 96 mm Hg, p < 0.01). Burn injury in the absence of vitamin therapy (group III) produced cardiac NF-kappaB nuclear migration 4 hours after burn and cardiomyocyte secretion of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 by 24 hours after burn. Antioxidant therapy in burns (group IV) improved cardiac function, producing left ventricular pressure and +/-dP/dt (82 +/- 2 mm Hg, 1,880 +/- 44 mm Hg, and 1,570 +/- 46 mm Hg/s) comparable to those measured in shams. Antioxidant vitamins in burns inhibited NF-kappaB nuclear migration at all times after burn and reduced burn-mediated cytokine secretion by cardiomyocytes. CONCLUSION: These data suggest that antioxidant vitamin therapy in burn trauma provides cardioprotection, at least in part, by inhibiting translocation of the transcription factor NF-kappaB and interrupting cardiac inflammatory cytokine secretion.

Animals↗
PubMed2002

Effects of burns on inhalation injury in sheep: a 5-day study.

BACKGROUND: We have previously reported that infliction of thermal injury immediately after smoke exposure did not accentuate pulmonary dysfunction during the subsequent 48 h. The purpose of this study was to determine whether thermal injury would aggravate pulmonary dysfunction during a longer postinjury period of 5 days. METHODS: Six sheep (G1) received 12 units of smoke inhalation injury (SII) alone; seven sheep (G2) received a 40% full-thickness scald burn immediately after SII. All sheep were resuscitated with lactated Ringer's solution for the first 48 h. After 48 h, animals were fed food and water ad libitum. Cardiopulmonary variables and blood gases were measured serially. At the end of the 5-day experimental period, VA/Q distribution was analyzed using the multiple inert gas elimination technique (MIGET). Lung wet to dry (W/D) weight ratios and malondialdehyde (MDA) concentrations were determined. RESULTS: Cardiac index in G2 significantly increased and remained higher compared with G1. There was no difference in A-aDO(2) between the two groups. There was also no difference between the two groups by MIGET study, or in terms of lung MDA and W/D weight ratios. None of the animals manifested symptoms of infection. CONCLUSION: Despite the difference in the hemodynamic changes induced by the addition of a 40% burn to smoke inhalation injury, pulmonary dysfunction was not accentuated during the 5-day study period in the absence of infection.

Analysis of Variance↗
PubMed2002

Granulocyte colony-stimulating factor: release is not impaired after burn wound infection.

BACKGROUND: The production of granulocyte colony-stimulating factor (G-CSF), the lineage specific essential regulator of neutrophil progenitor cell proliferation and differentiation, has been thought to be impaired in the setting of burn infection. The ability to directly measure murine G-CSF allows the further delineation of the G-CSF response in a clinically relevant model of thermal injury and infection. METHODS: We used a commercially available solid phase enzyme-linked immunoabsorbent assay to quantify G-CSF production after burn wound infection in mice. Bone marrow cells, splenic cells, and serum were obtained from BDF1 mice on day 3 after a 15% total body surface area full-thickness scald burn with or without Pseudomonas aeruginosa burn wound infection. G-CSF production of bone marrow cells or splenic cells and the serum level of G-CSF were measured. A clonogenic assay of bone marrow and spleen granulocyte-macrophage progenitor cells as well as blood leukocyte counts were also performed. RESULTS: After burn sepsis, we noted that G-CSF production of the bone marrow and spleen was significantly increased; the numbers of progenitor cells in bone marrow and spleen were markedly enhanced; serum values of G-CSF were 14 times greater than control values; serum colony-stimulating activity was greater than in control mice; and total blood leukocyte counts were significantly depressed. CONCLUSION: These findings support the notion that granulocytopoietic failure after burn sepsis is not significantly related to defective endogenous G-CSF synthesis. More likely, hyporesponsiveness of granulocyte progenitor cells to G-CSF, changes in the relative balance of granulocyte versus monocyte progenitors within the granulocyte-macrophage progenitor cell compartment, and enhanced release of monocyte lineage specific growth factors are the critical elements responsible for burn infection-induced hematopoietic failure.

Analysis of Variance↗
PubMed2002

Lipopolysaccharide-binding protein and lipopolysaccharide receptor CD14 gene expression after thermal injury and its potential mechanism(s).

BACKGROUND: We hypothesized that lipopolysaccharide-binding protein (LBP) and lipopolysaccharide receptor CD14 would present a pair of key molecules in pathophysiologic alterations induced by low concentrations of endotoxin after trauma. The aim of this study was to investigate the relationship between endotoxin translocation and tissue LBP/CD14 messenger ribonucleic acid (mRNA) expression after burn injury, and to define the potential role of LBP/CD14 in mediating inflammatory mediator induction, as well as the pathogenesis of organ damage. METHODS: Wistar rats were subjected to a 35% full-thickness scald injury, and tissue samples from liver, kidneys, lungs, and intestine were collected to measure LBP/CD14 and tumor necrosis factor-alpha (TNF-alpha) mRNA expression. Peritoneal macrophages were harvested by peritoneal lavage to determine CD14 mRNA expression. RESULTS: It was found that endotoxin levels in liver, spleen, and lung increased markedly after thermal injury, with the highest level in liver. Both tissue LBP and CD14 mRNA expression increased markedly after burns, peaking at 12 hours, and then decreasing gradually. At 48 hours, LBP gene expression had a tendency to the baseline level, whereas CD14 mRNA expression increased again. Likewise, CD14 mRNA levels were up-regulated markedly in peritoneal macrophages. Conversely, gene expression of TNF-alpha in tissues elevated markedly after acute insults. There were positive correlations between lipopolysaccharide levels and LBP/CD14 mRNA as well as TNF-alpha mRNA expression in tissues. Similar results were also obtained between CD14, TNF-alpha mRNA expression in liver tissue and liver function parameters, and between pulmonary TNF-alpha mRNA and myeloperoxidase activities (p < 0.01). CONCLUSION: Thermal injury per se can markedly up-regulate both LBP and CD14 gene expression in various organs. Excessive LBP and CD14 mRNA expression might be associated with enhanced synthesis and release of TNF-alpha stimulated by endotoxin translocation after major burns.

Acute-Phase Proteins↗
PubMed1982

Progression of thermal injury: a morphologic study.

The events that participate in the local pathophysiology of a burn would have not been completely described. This study defines the sequential morphologic changes following untreated partial-thickness burns. Guinea pigs received partial-thickness scald burns by 75 degrees C water immersion for 10 seconds. Skin samples were then obtained at 2, 8, 24, and 96 hours after the burn and examined by light and electron microscopy. A definite progression of the thermal injury was found, with maximum tissue destruction occurring 8 hours after the burn. At 24 hours after the burn, some improvement in the burn wound was noted, especially in the dermal microvasculature. At 96 hours, the damaged epidermis sloughed, exposing a dermis that contained areas resembling microabscesses.

Animals↗
PubMed1999

The use of skin grafts in postburn contracture release: a 10-year review.

Postburn scarring and contracture affecting function remain the most frustrating late complications of burn injury. Various techniques are used to release contractures; the choice depends on their location and/or the availability of unaffected skin adjacent to the contracture or elsewhere. A retrospective review was carried out of the case notes of patients who had skin grafting for the release of postburn contracture at the Burns Unit, City Hospital, Nottingham between May of 1984 and August of 1994 to evaluate the experience over this period. Information was obtained about the burn injury, contracture site, interval between burn and release of contracture, indication, age at first release, intervals between releases, operative details (donor and graft sites), complications and nonoperative treatment, and follow-up to the end of the study period. A total of 129 patients underwent skin grafting for release of contractures as opposed to any other method of correction. Full-thickness skin grafts were used in 81 patients (63 percent) and split-thickness skin grafts in 26 (20 percent). Twenty-two patients (17 percent) had both types used on different occasions. Flame burns (41 percent) were the most common causes, followed by scalds (38 percent). Two hundred thirty-nine sites of contracture were released, with the axilla (59) and the hand/wrist (59) being the most common sites involved, followed by the head/neck region (42). It was found that for the same site, release with split-thickness skin grafts was associated with more rereleases of the contracture than with full-thickness skin grafts. Also, the interval between the initial release and first rerelease was shorter than with full-thickness skin grafts (p < 0.048). It was also noted that children required more procedures during growth spurts, reflecting the differential effect of the growth of normal skin and contracture tissue. Patients reported more satisfaction with texture and color match with the full-thickness skin grafts. There was comparable donor-site and graft morbidity with both graft types. The use of skin grafts is simple, reliable, and safe. Whenever possible, the authors recommend the use of full-thickness skin grafts in preference to split-thickness skin grafts in postburn contracture release.

Adolescent↗
PubMed2002

Improvement in burn wound infection and survival with antimicrobial peptide D2A21 (Demegel).

Naturally occurring antimicrobial peptides have been discovered in both plants and animals. Many of these peptides demonstrate impaired activity or cytotoxicity when applied exogenously. Synthetically engineered antimicrobial peptides have been designed to increase potency and activity against bacteria and fungus yet remain noncytotoxic. The antimicrobial peptide D2A21 (Demegel) has already demonstrated significant activity in vitro against many common hospital pathogens. The purpose of this study was to evaluate the effects of D2A21 in an in vivo infected burn-wound model, examining both quantitative cultures of the wound and survival of the animal. Forty-four Wistar rats were subjected to a 23 percent total body surface area scald burn. Pseudomonas aeruginosa was administered topically with 108 organisms and wounds were then evaluated at day 1, 2, or 3 for eschar and subeschar muscle quantitative culture. The experimental group was treated daily with 1.5% topical D2A21. The control group was treated with control gel. A second group of Wistar rats (n = 14) were burned and given a 107 inoculum of the same Pseudomonas and evaluated to 14 days for survival and weight changes. This group was subdivided into rats receiving either topical D2A21 or control base daily. The quantitative biopsy results demonstrated that D2A21-treated wounds had no bacterial growth in burn eschar at day 2 or 3, whereas control animals demonstrated growth at greater than 105 organisms by day 2. Subeschar muscle cultures also demonstrated significantly less bacterial invasion compared with controls on each day tested. D2A21-treated animals had an 85.7 percent survival compared with 0 percent survival in controls. Furthermore, the D2A21-treated groups demonstrated maintenance of body weights, whereas controls had significant weight loss with time. In conclusion, D2A21 demonstrates significant antibacterial activity against Pseudomonas, sterilizing burn eschar and decreasing subeschar bacterial load, allowing for a markedly significant improvement in survival in this infected burn-wound model.

Animals↗
PubMed1985

Survey of childhood burns in Hawaii.

A review of 247 pediatric emergency charts and 80 pediatric impatient charts was performed over a three-year period at a tertiary care children's hospital in Honolulu. The purpose of this review was to examine the causes of childhood burns in Hawaii in order to develop guidelines for anticipatory guidance regarding burn prevention. Most burns occurred in the 0.8- to 3.0-year age group. Over one half of these burns were caused by tap water. Medicaid patients were more likely to be admitted to the hospital than nonMedicaid patients. Severe burns were mainly the result of scalds, fire, or contact with heating appliances. Burn severity and the causes of burns did not vary significantly with sex or ethnic or economic status. A burn prevention program which adequately addresses the unique cultural and climatic differences of this community, based on the data obtained, is described.

Accidents, Home↗
PubMed1994

Burn injuries among children in an urban emergency department.

To determine the profile of burn injury among an ambulatory population, we conducted a retrospective chart review over a one-year period of all first visits by patients under age 18 receiving burn care in our emergency department. Of the 109 visits, contact burns were most numerous (43.1%) followed by scalds (33.9%), flame/explosion (11.0%), cigarettes (5.5%) and electrical (2.8%). For children under 11 years of age, contact burns caused over half of all burns. Irons accounted for 44.7% of contact burns and 19.1% of all burns. The next most frequent causative agents were beverages (14.7%), food (nonbeverage) (7.3%), tap water/bath (7.3%), and cooking-related (6.4%). Contact burns were more likely to be smaller and more localized when compared with other burns. The cause and causative agents of burns differ in frequency and relative importance depending on the patient population studied and the level of medical care being provided. Specific burn prevention strategies should be directed toward particular patterns of injury within defined patient groups.

Burns↗
PubMed1988

Cyclosporine and skin allografts for the treatment of thermal injury. II. Development of an experimental massive third-degree burn model demonstrating extensive graft survival.

We have previously reported the successful treatment and apparent development of skin allograft tolerance in a patient sustaining massive burns, utilizing skin allografts and cyclosporine. We now report the experimental correlate via successful achievement of a 75% body surface area (BSA) scald burn cyclosporine-skin allograft model in Lewis (LEW) rats. Cyclosporine (8 mg/kg/day) was given to the experimental animals daily for the first 20 days and then three times a week thereafter. Two experimental groups were studied: one received standard posttrauma care and the second critical posttrauma care. Controls (n = 22) and experimental groups 1 (n = 28) and 2 (n = 4) had average survival times of 13.8 +/- 12.8 days, 44.2 +/- 132.5 days, and 172.0 +/- 19.4 days, respectively. The allografts on the surviving experimental animals appeared normal and healthy and had nearly perfect hair growth. These results indicate that the model follows the clinical burn wound course, and treatment of massive burns with primary excision, skin allografts, and low doses of cyclosporine could provide immediate and complete functional repair of the burn wound.

Animals↗
PubMed2002

Toxic epidermal necrolysis after phenytoin usage in a brain trauma patient.

Toxic epidermal necrolysis is a drug-induced, rare, but life-threatening skin eruption. The main differential diagnoses are drug-induced erythema (hypersensitivity syndrome), acute graft-versus-host disease, staphylococcal scalded skin syndrome, and toxic shock syndrome. Because the therapy for toxic epidermal necrolysis and acute graft-versus-host disease differs largely from the others, it is necessary to make an accurate diagnosis. In addition to a detailed medical history, skin biopsy is mandatory because the skin eruptions are not always unequivocal. Discontinuation of the causing agent is crucial, and treatment in specialized intensive care units or burn units is supportive. Currently there is no specific treatment for toxic epidermal necrolysis. Advantages from corticosteroids, plasmapheresis, intravenous immunoglobulin, cyclophosphamide, cyclosporin, and N-acetylcysteine still remain to be established by controlled trials, or have failed to prove a benefit (thalidomide). The patient presented here demonstrates the difficulties in diagnosing toxic epidermal necrolysis in a critically ill patient. A short overview of the pathogenesis and the management of toxic epidermal necrolysis is provided.

Accidents, Traffic↗
PubMed1994

L-arginine improves resting cardiac transmembrane potential after burn injury.

Previous studies from our laboratory have suggested that burn injury disrupts nitric oxide production and promotes a loss of cell membrane integrity. We hypothesized that administration of L-arginine, a precursor of nitric oxide (NO), would prevent postburn depolarization of the cardiac cell membrane and preserve cell membrane integrity. Third degree scald burn comprising 43% of the total body surface area was produced in rats (n = 22); sham burn controls (n = 11) were included. Burn rats were either untreated (N = 11) or given 300 mg/kg L-arginine immediately, 3, 6, and 23 h postburn. Untreated burn injury caused depolarization of the cardiac cell membrane (cardiac Em fell from 79.0 +/- 1.4 mV in shams to 67.0 +/- 1.5 mV 24 h after untreated burn, p < .05) and an increase in myocardial tissue lactate. Urine nitrate levels (assessed to provide a measure of NO production) fell after untreated burn (0.49 +/- 0.10 microM/24 h) compared with levels measured in sham burns (7.99 +/- 0.64 microM/24 h, p < .05), indicating that burn injury reduced NO production. Postburn administration of L-arginine improved cardiac Em (81.5 +/- 2.1 mV), reduced myocardial tissue lactate levels, and increased urinary nitrate levels above values measured for untreated burns. Our data indicate that L-arginine, in the absence of fluid resuscitation, provides postburn cardiac cell membrane protection, possibly due to enhanced nitric oxide production.

Adenosine Triphosphate↗
PubMed1998

Thermal injury induces macrophage hyperactivity through pertussis toxin-sensitive and -insensitive pathways.

C57BL/6 mice were subjected to a full thickness scald thermal injury covering 25% of their total body surface area, and thioglycollate elicited peritoneal macrophages (Mphi were isolated 4 days later. Mphi from injured mice produced significantly greater amounts of reactive nitrogen intermediates and tumor necrosis factor-alpha in response to lipopolysaccharide and lipid A. Pertussis toxin (PTX) treatment of Mphi dose-dependently inhibited reactive nitrogen intermediate production in Mphi from sham-treated mice; however, Mphi from injured mice were insensitive to PTX-mediated inhibition. Conversely, tumor necrosis factor-alpha production was enhanced by PTX treatment, with Mphi from injured mice being more sensitive than Mphi from sham-treated mice to this effect of PTX. These results indicate that thermal injury increases Mphi sensitivity to lipopolysaccharide by a mechanism that is both PTX sensitive and PTX insensitive, thereby suggesting a role for G proteins in the modulation of Mphi activity after thermal injury.

Animals↗
PubMed1998

Acute ethanol exposure prior to thermal injury results in decreased T-cell responses mediated in part by increased production of IL-6.

Previous studies by our laboratory have demonstrated that acute ethanol exposure prior to thermal injury results in suppression of cellular immune responses when compared with thermal injury alone. Ethanol exposure and burn injury are independently known to result in elevated IL-6, a cytokine with potent immunosuppressive properties. Therefore, we examined the role of IL-6 in the immune dysfunction in mice following a 15% body surface area scald (or sham) injury combined with acute ethanol (or vehicle) treatment. At 24 h post-injury, we observed slightly suppressed splenocyte proliferative responses and elevated circulating IL-6 (149+/-15 pg/mL) in mice receiving burn alone compared with those receiving sham injury (31+/-7 pg/mL). In contrast, burn + ethanol treated mice showed a profound suppression of splenocyte proliferation (20% of control) and significantly elevated circulating IL-6 levels (738+/-218 pg/mL). The suppressed splenocyte proliferative response was found to be macrophage dependent. Furthermore, IL-6 production was significantly elevated (p < .05) in splenic macrophage cultures from burn + ethanol mice (159+/-6 pg/mL) when compared with burn alone (109+/-10 pg/mL). Treatment of the splenocyte cultures from burn + ethanol mice with an anti-IL6 monoclonal antibody resulted in partial restoration of splenocyte proliferation. Taken together, these data strongly suggest that the immune dysfunction observed in ethanol-exposed, thermally injured mice is mediated in part by elevated levels of IL-6.

Alcohol Drinking↗
PubMed1999

Major burn trauma in rats promotes cardiac and gastrointestinal apoptosis.

The hypothesis that cardiac functional abnormalities that occur after major burn trauma are paralleled by an increased incidence of apoptosis in cardiac myocytes was examined. Adult Sprague-Dawley rats were given a full thickness scald burn comprising 43+/-1% of the total body surface area or were manipulated identically but not exposed to burn injury (sham burn); burned rats were fluid resuscitated with lactated Ringer's solution. Tissues from burn and sham burn animals were then examined by the TUNEL (TdT-mediated dUTP nick end labeling) assay and light microscopy to determine the presence of apoptosis 24 and 48 h after burn trauma. In parallel, the mechanical function of the heart was assayed in separate groups of rats. Tissues harvested from the hearts of sham-treated animals showed essentially no apoptosis, whereas a small number of apoptotic cells were noted in the intestinal villi and liver of sham-treated animals. Twenty-four hours after burn trauma, there was a marked increase in apoptotic cells in the left ventricle (+916%), and the number of apoptotic cells remained increased by eightfold 48 h postburn. Apoptosis was noted predominately in the subendocardial tissue of the left ventricle. The appearance of apoptotic cells was paralleled by a decrease in cardiac mechanical function with significant decreases in left ventricular pressure and +/-dP/dt(max). Burn injury also increased apoptosis in the small intestine significantly, whereas apoptosis in the liver did not increase with burn trauma. These data suggest that the apoptosis of the cardiac myocytes that occurs after burn trauma may contribute, in part, to postburn cardiac mechanical dysfunction.

Animals↗