Showing papers by "Shriners Hospitals for Children - Galveston published in 2001"

Reversal of catabolism by beta-blockade after severe burns.

Abstract: Background The catecholamine-mediated hypermetabolic response to severe burns causes increased energy expenditure and muscle-protein catabolism. We hypothesized that blockade of β-adrenergic stimulation with propranolol would decrease resting energy expenditure and muscle catabolism in patients with severe burns. Methods Twenty-five children with acute and severe burns (more than 40 percent of total body-surface area) were studied in a randomized trial. Thirteen received oral propranolol for at least two weeks, and 12 served as untreated controls. The dose of propranolol was adjusted to decrease the resting heart rate by 20 percent from each patient's base-line value. Resting energy expenditure and skeletal-muscle protein kinetics were measured before and after two weeks of beta-blockade (or no therapy, in controls). Body composition was measured serially throughout hospitalization. Results Patients in the control group and the propranolol group were similar with respect to age, weight, percentage of tota...

Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise

Abstract: The present study was designed to determine whether consumption of an oral essential amino acid-carbohydrate supplement (EAC) before exercise results in a greater anabolic response than supplementa...

Effects of a 12-wk resistance exercise program on skeletal muscle strength in children with burn injuries

Abstract: The posttraumatic response to burn injury leads to marked and prolonged skeletal muscle catabolism and weakness, which persist despite standard rehabilitation programs of occupational and physical therapy. We investigated whether a resistance exercise program would attenuate muscle loss and weakness that is typically found in children with thermal injury. We assessed the changes in leg muscle strength and lean body mass in severely burned children with >40% total body surface area burned. Patients were randomized to a 12-wk standard hospital rehabilitation program supplemented with an exercise training program (n = 19) or to a home-based rehabilitation program without exercise (n = 16). Leg muscle strength was assessed before and after the 12-wk rehabilitation or training program at an isokinetic speed of 150 degrees /s. Lean body mass was assessed using dual-energy X-ray absorptiometry. We found that the participation in a resistance exercise program results in a significant improvement in muscle strength, power, and lean body mass relative to a standard rehabilitation program without exercise.

Attenuation of posttraumatic muscle catabolism and osteopenia by long-term growth hormone therapy.

Abstract: The hypermetabolic response to severe trauma is associated with increased systemic energy expenditure, peripheral insulin resistance, immunodeficiency, and marked whole body catabolism. These systemic derangements are most profound after severe burn. Classically, hypermetabolism associated with injury was thought to recede with closure of wounds and healing of bone and soft tissue injury. 1,2 In our long-term follow-up of severely burned children, however, we found that hypermetabolism did not abate after full healing of burn wounds; in fact, we found that children burned over 40% total body surface area (TBSA) undergo muscle protein catabolism for at least 9 months 3 and growth arrest for at least 2 years after injury. 4 The clinical result of this persistent pathology is wasting of musculature at a time when strength reserves would be of benefit to assist with recovery, rehabilitation, and reintegration into society. Growth hormone is known to be a potent anabolic agent and salutary modulator of posttraumatic metabolic responses. 5 After severe burn, it has been shown to decrease whole body catabolism, 6 improve muscle protein synthesis, 7 accelerate wound healing, 8,9 attenuate prolonged hyperactivity of the hepatic acute-phase response, 10,11 and promote linear growth. Its side effects when used in burned children are well characterized, and it has been shown to be a safe pharmacotherapeutic adjunct to standard excisional therapy after severe burn. 12,13 The purpose of this study was to determine whether the effects of growth hormone after severe burn persist throughout the prolonged hypermetabolic and hypercatabolic response to severe burn. Specifically, our hypothesis was that low-dose growth hormone increases accretion of muscle mass and attenuates bone mineral wasting when given daily during outpatient convalescence, from hospital discharge through 1 year after severe burn.

Liposomal IGF-1 gene transfer modulates pro- and anti-inflammatory cytokine mRNA expression in the burn wound.

Abstract: Liposomal IGF-1 gene transfer modulates pro- and anti-inflammatory cytokine mRNA expression in the burn wound

The effects of exercise programming vs traditional outpatient therapy in the rehabilitation of severely burned children

Abstract: The purpose of this study was to compare the efficacy and effects of exercise programming (Study group, n = 11) vs traditional outpatient therapy (Home group, n = 10) in burned children (> 40% body surface area). This was a prospective, randomized, controlled trial in a hospital-based children's wellness center. Twenty-one patients (13 boys and 8 girls) averaging 10.6 +/- 0.9 years and TBSA = 59.7 +/- 3.1% were evaluated 6 and 9 months postburn. Moderate intensity, progressive resistance and aerobic exercise conducted 3 times weekly for 1 hour were a supplement to standard therapy over 12 weeks. Muscular strength and functional outcome significantly increased in both groups (P < .05). Improvements in strength (80.1 vs 37.7%) and distance walked (39.5 vs 12.5%) were significantly greater for Study vs Home groups, respectively, P < .05. We conclude that exercise programming may be safely included in rehabilitation programs for severely burned children and can be effective in increasing muscular strength and functional outcome.

Glucan phosphate potentiates endotoxin-induced interferon-γ expression in immunocompetent mice, but attenuates induction of endotoxin tolerance

Abstract: Glucan phosphate has been shown to enhance antimicrobial immunity in a variety of experimental models. However, the mechanisms by which glucans enhance resistance to infection remain largely unknown. Interferon-γ (IFN-γ) is a key regulator of both innate and acquired immunity. Suppression of IFN-γ production is a prominent feature of the altered immune response that follows major trauma or sepsis. The present studies were designed to determine the effect of glucan phosphate on IFN-γ expression in normal mice and endotoxin [lipopolysaccharide (LPS)]-tolerant mice. The model of LPS tolerance was used because it results in patterns of cytokine expression similar to those commonly observed following severe trauma or sepsis. Glucan treatment potentiated LPS-induced IFN-γ expression in control mice. The induction of LPS tolerance resulted in marked suppression of LPS-induced IFN-γ production. However, co-administration of glucan with LPS, during the tolerance induction phase, attenuated the LPS-tolerant response. Interleukin-12 (IL-12) and IL-18 are important mediators of LPS-induced IFN-γ production. LPS-induced IL-12 p40 mRNA expression was increased in the spleens of glucan-treated mice compared with controls. Induction of LPS tolerance caused marked suppression of IL-12 production, a response that was attenuated by glucan treatment. IL-18 was constitutively expressed in both control and LPS-tolerant mice, and LPS-induced serum levels of IL-18 were increased in mice treated with glucan. T cells isolated from glucan-treated mice exhibited increased IFN-γ expression in response to IL-12 and IL-18, as well as increased expression of the IL-12 and IL-18 receptors. The ability of glucan to potentiate IFN-γ expression in control mice provides a potential mechanism by which glucan enhances antimicrobial immunity. The ability of glucan to attenuate suppressed IFN-γ expression in LPS-tolerant mice denotes its potential benefit for the treatment of trauma and sepsis-induced immunosuppression.