Calpains are intracellular nonlysosomal Ca(2+-) regulated cysteine proteases, widely located in the tissues of most mammals. Skeletal muscle tissue mainly expresses m-calpain, µ-caplain, n-calpain, and their endogenous inhibitor calpastatin. They are closely related to the cell apoptosis, cytoskeleton formation, cell cycles, etc. Calpains are also considered to be participating in the protein degradation process. Severe burns are typically followed by hypermetabolic responses that are characterized by hyperdynamic circulatory responses with increased proteolysis and cell apoptosis. Recently, overloading of Ca(2+) in skeletal muscle cells, which activates the calpains is observed after a serious burn. This paper aims to review the current research of the relationship between calpains and post-burn skeletal muscle wasting from the perspectives of structure, function, and physiological activities.
Animals ; Burns ; metabolism ; pathology ; Calpain ; metabolism ; Muscle, Skeletal ; metabolism ; pathology

Burns ; complications ; metabolism ; Humans ; Inflammation ; etiology ; metabolism ; prevention & control

Most of the major advances in burn treatment were made within the last five decades. However, hypermetabolic response after severe burn remains a problem in the treatment of patients with massive burn. As skeletal muscle accounts for over 50% of body cell dry weight, its catabolism exerts profound effect on body metabolism as a whole. Main mechanisms underlying skeletal muscle wasting induced by severe burn include activation of ubiquitin-proteasome pathway, bringing about breakdown of muscle protein, and myonuclear apoptosis. Therapeutic strategies for skeletal muscle wasting after burn mainly include maintenance of room temperature at (31.5 +/- 0.7) degrees C, early active and passive exercise of skeletal muscles, administration of beta adrenergic receptor blocker such as Propranolol, recombinant growth hormone, androgen, and insulin, which has lately been proven to possess the effect of suppressing myonuclear apoptosis after burn. Combination of multiple therapeutic strategies is beneficial in reducing complications of burn patients, particularly wide ranged skeletal muscle atrophy, to achieve a better clinical outcome.
Apoptosis ; Burns ; drug therapy ; metabolism ; pathology ; Humans ; Muscle, Skeletal ; metabolism

After a series of study of early feeding (EF), we consider the evaporative heat loss from the burn wound is not the main mechanism of burn hypermetabolism. EF could resuscitate the intestine, preserve its structural integrity and function, prevent bacterial translocation and release of inflammatory mediators, reduce muscle protein catabolism and hypermetabolism. Our studies concerning the relationship between EF and hypermetabolism have already extended to involve hypothalamus now. At the end of 1960s, the advancement in "Intravenous Hyperalimentation" has epoch-making significance, but it has been found later that energy has been oversupplied by this measure, thus it exacerbated visceral loading and led to disorder of internal environment, and it has been found not beneficial to alleviate hypermetabolism. Whether "hypocaloric nutrition" for post-operative patients of G-I (gastro-intestine) surgery is applicable to severe burn patients remains as a problem. Some specialists suggest it is better to supply 126 approximately 146 kJxkg(-1)x d(-1) in severe burn patients. After evaluating the bias and precision of 46 methods of estimating energy supply of burn patients reported from 1953 to 2000, Dickerson RN et al. concluded that the most precise, unbiased methods were those of Milner (1994), Zawacki (1970) and TMMU (1993, Third Military Medical University formula). Though formulas are simple and convenient to estimate energy supplementation, however, it is difficult to evaluate the requirement of energy when the patient's condition changes immensely.
Burns ; metabolism ; therapy ; Energy Metabolism ; Humans ; Nutritional Support

The energy expenditure of burn patients can be determined accurately by indirect calorimetry measurement, or estimated approximately with energy expenditure equations. However, the energy requirement is not entirely equal to energy expenditure in the whole process of burn injury. The energy consumption induced by hyper catabolism is increased significantly, and on the other hand, the ability of nutrient absorption and anabolism decreased remarkably in the early phase of burn injury, thus leading to imbalance between energy consumption and demand. However, energy supplement as calculated according to energy consumption may induce overfeeding in the early phase of burn injury. Excessive nutrients intake can not be fully utilized to decrease hypermetabolic reaction, but it might exacerbate metabolic disorder. Therefore, the energy supplement should be lower than energy consumption during the early stage of burns. With the advance of disease course, the internal environment becomes stable gradually, ending in a balance between anabolism and catabolism. Energy supplement should be increased gradually according to energy consumption. During the convalescent period, anabolic metabolism exceeds catabolic metabolism, therefore the quantity of energy supplement should be moderately higher than that of energy consumption. Thus, the energy consumption and energy supplement may reach a balance during the whole course of treatment. The purpose of the article is to analyze and discuss how to estimate energy expenditure precisely and evaluate energy requirement correctly, in order to reach a balance between energy consumption and supplement during a long course of treatment for severe burn patients.
Burns ; metabolism ; therapy ; Energy Metabolism ; Humans ; Nutritional Support ; Oxygen Consumption

OBJECTIVETo investigate the characteristics and differences of propofol pharmacokinetics in shock phase and hypermetabolic phase in severe burn in rabbits.

METHODSTwenty New Zealand rabbits were assigned to burn group (n = 10) and sham injury group (n = 10) according to the random number table. Rabbits in burn group were inflicted with 30%TBSA full-thickness scald (named burn below), resuscitated instantly, and were intravenously injected with 5.1 mg/kg propofol 6 hours after injury. 1.5 mL blood was collected from left external jugular vein at 1, 3, 5, 10, 15, 20, 30, 45, 60, 90 minute(s) after injection respectively. Above procedure was performed again 1 week later. Rabbits in sham injury group were treated similarly as rabbits in burn group but were sham scalded. Propofol concentration in plasma was determined with high performance liquid chromatography. Data of propofol concentration-time were analyzed with 3P97 practical pharmacokinetics calculating program, and then the most fit compartment model was selected to calculate pharmacokinetic parameters.

RESULTSThe blood concentration-time curve of propofol fitted in with the two-compartment model in burn group, and three-compartment model in sham injury group. During shock phase, comparing with central compartment distribution volume [Vc, (3.1 + or - 1.5) L/kg], area under curve [AUC, (25 + or - 7) mg x min x L(-1)], elimination phase half life [t1/2beta, (113 + or - 93) min], clearance [CLs, (110 + or - 50) mL x kg(-1) x min(-1)] of rabbits in sham injury group, Vc[(8.8 + or - 4.2) L x kg(-1)] and AUC [(44 + or - 10) mg x min x L(-1)] increased significantly (with t value respectively 3.191 and 3.668, and P values both below 0.01); t1/2beta [(339 + or - 258) min] prolonged (t = 2.932, P < 0.05); CLs [(40 + or - 30) mL x kg(-1) x min(-1)] decreased (t = -3.013, P < 0.05) in burn group. During hypermetabolic phase, CLs [(180 + or - 40) mL x kg(-1) x min(-1)] of rabbits in burn group was significantly higher than that in sham injury group [(90 + or - 30) mL x kg(-1) x min(-1), t = -3.013, P < 0.05]. Comparing with those of rabbits in burn group during shock phase, Vc [(4.1 + or - 1.3) L/g] and AUC [(24 + or - 5) mg x min x L(-1)] decreased significantly (with t value respectively 2.979 and 3.766, and P value both below 0.01); distribution phase half time [t1/2alpha, shock phase (16.1 + or - 13.1) min and hypermetabolic phase (8.3 + or - 2.5) min] and t1/2beta [(55 + or - 19) min] shortened obviously (with t value respectively 9.065 and 8.795, and P values both below 0.01); CLs increased significantly (t = 4.238, P < 0.01) during hypermetabolic phase.

CONCLUSIONSThere are great differences in propofol pharmacokinetics between shock phase and hypermetabolic phase in severely burned rabbits. The change is characterized by increase in Vc and AUC, extension of t1/2alpha and t1/2beta, decrease in CLs during shock phase and obvious increase of CLs during hypermetabolic phase.

Animals ; Burns ; metabolism ; pathology ; Propofol ; pharmacokinetics ; Rabbits ; Shock ; metabolism

OBJECTIVETo observe the expression of laminin and fibronectin in alkali-burned corneas in rats.

METHODSA total of 18 normal Wistar rats were randomly divided into 6 groups (n = 3 in each group). For each rat, one eye was injured by alkali burn, the other one was taken as the normal control. Then all the corneas were surgically removed and the expression of laminin and fibronectin was observed with immunohistochemistry respectively at 7 hours, 1 day, 3 days, 7 days, 14 days and 28 days after alkali burn.

RESULTSCompared with that of the normal controls, the expression of laminin and fibronectin of the burned eyes was dramatically higher at 7 hours, reached peak at 14 days and decreased to the normal level at 28 days after alkali burn.

CONCLUSIONSIn the process of wound healing after alkali burn, the expression of laminin and fibronectin increases dramatically, which suggests that laminin and fibronectin may participate in the process of corneal wound healing.

Animals ; Burns, Chemical ; metabolism ; Corneal Injuries ; Eye Burns ; metabolism ; Fibronectins ; metabolism ; Immunohistochemistry ; Laminin ; metabolism ; Rats ; Rats, Wistar ; Wound Healing ; physiology

Burns ; complications ; metabolism ; Endotoxemia ; etiology ; metabolism ; Humans ; Multiple Organ Failure ; etiology ; metabolism ; Myocytes, Cardiac ; metabolism

OBJECTIVETo observe the structural and functional changes in islet beta cells in severely scalded rats, and to explore its relationship with dysfunction of glycometabolism.

METHODSSeventy-two Wistar rats were divided into scald (S) group and sham injury (SI) group according to the random number table, with 36 rats in each group. Rats in group S were inflicted with 50%TBSA full-thickness scald by a 12-s immersion of back and a 6-s immersion of abdomen in 94 °C hot water. Rats in group SI were sham injured through immersion of back and abdomen in 37 °C warm water. At post injury hour (PIH) 6 and on post injury day (PID) 3 and 7, plasma glucose level was measured for intraperitoneal glucose tolerance test (IPGTT) in 12 rats of each group, and the area under the curve (AUC) of plasma glucose level was calculated. After the IPGTT, pancreatic tissue was harvested and subjected to a double immunostaining for insulin and cell nuclei to determine the pancreatic insulin-positive area ratio, and the area and number of beta cells in the islets (referred to as "the three indicators in the islets"). Data were processed with the analysis of repeated measures and factorial designed analysis of variance, and LSD test was applied for paired comparison.

RESULTS(1) At PIH 6 and on PID 3, the overall plasma glucose levels of rats in group S before and after injection of glucose and at each time point were obviously higher than those of rats in group SI (with F values of main effects respectively 79.372 and 32.962, P values all below 0.001; with P values of paired comparison below 0.05 or 0.01). On PID 7, the overall plasma glucose levels in the two groups before and after injection of glucose and at each time point were close (with P values all above 0.05). (2) The overall AUC of plasma glucose levels of rats in group S was higher than that of rats in group SI (main effects: F = 337.87, P < 0.01). Compared with those of rats in group SI [(1019 ± 32), (1003 ± 72) mmol·min·L(-1)], the AUCs of plasma glucose levels of rats in group S were higher at PIH 6 and on PID 3 [(1501 ± 163), (1132 ± 67) mmol·min·L(-1), P values all below 0.001]. The AUCs of plasma glucose levels were close between two groups on PID 7 (P > 0.05). The AUCs of plasma glucose levels on PID 3 and 7 were both lower than that at PIH 6 in rats of group S (with P values all below 0.001). (3) The three indicators in the islets in rats of group S were all lower than those of rats in group SI (with F values of main effects respectively 135.17, 24.75 and 39.35, P values all below 0.01). There were no significant differences in the three indicators in the islets at PIH 6 between two groups (with P values all above 0.05). The three indicators in the islets of rats in group S on PID 3 and 7 [0.47 ± 0.05, 0.51 ± 0.07; (0.032 ± 0.008), (0.037 ± 0.008) mm(2); (303 ± 64), (341 ± 58) cells] were significantly lower than those of rats in group SI [0.63 ± 0.05, 0.64 ± 0.06; (0.043 ± 0.011), (0.044 ± 0.012) mm(2); (398 ± 112), (387 ± 90) cells; P < 0.05 or P < 0.01] and that at PIH 6 within group S (P < 0.05 or P < 0.01).

CONCLUSIONSThe number of beta cells is reduced, and the insulin secretion function of beta cells is decreased in the scalded rats, and they may constitute the cause of dysfunction of glycometabolism, mainly manifested as hyperglycemia.

Animals ; Blood Glucose ; metabolism ; Burns ; metabolism ; Insulin ; metabolism ; Insulin-Secreting Cells ; metabolism ; Male ; Rats ; Rats, Wistar

Severe burns evoke a substantial metabolic response causing physiological derangement leading to a hyper-metabolic state. The hyper-metabolic response is accompanied by severe catabolism and a loss of lean body mass and also by a progressive decline of host defenses that impairs the immunological response. The protective functions of an intact skin are lost, leading to increased risk of infection and protein loss. Therefore, nutritional therapy is a cornerstone of burn care from the early resuscitation phase to the end of rehabilitation. Careful assessment of the nutritional state of the burn patient is also important to reduce infection and recovery time, and improve long-term outcomes. Evidence-based research has shown that nutritional therapy contributes to improved clinical outcomes.
Burns* ; Humans ; Metabolism ; Nutrition Therapy* ; Rehabilitation ; Resuscitation ; Skin