glycogen and Burns

Topics: Adaptation, Physiological; Burns; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Enteral Nutrition; Fats; Fractures, Bone; Glycogen; Humans; Metabolic Clearance Rate; Nutrition Disorders; Nutritional Physiological Phenomena; Parenteral Nutrition; Parenteral Nutrition, Total; Peritonitis; Postoperative Care; Postoperative Complications; Proteins

Topics: Adenosine Triphosphate; Adrenal Glands; Burns; Endocrine Glands; Glycogen; Glycolysis; Heart; Humans; Kidney; Lipid Metabolism; Liver; Lung; Metabolic Diseases; Minerals; Proteins; Water-Electrolyte Balance

The hypermetabolic response to burn increases protein catabolism. Euglycemic hyperinsu-linemia with exogenous insulin maintains muscle protein by continued stimulation of net protein synthesis. Our aim was to determine the effect of euglycemic hyperinsulinemia over the entire hospitalization on muscle anabolism by investigating lean body mass (LBM) as the primary endpoint.. Eighteen subjects between the ages of 2 and 18 with burns of more than 40% were prospectively randomized into 2 groups, a control (n = 9) and a treatment group (n = 9). The treatment group was given continuous intravenous insulin at a rate of at least 1.5 microU/kg/min to maintain serum glucose levels between 100 to 140 mg/dL. Treatment was instituted 24 to 48 hours after arrival and continued until the patient's injury was 95% healed. All patients received continuous enteral feeding. Patients underwent body composition studies by dual-energy x-ray absorptiometry (DEXA) scan on postoperative day 6 after initial burn excision and when 95% healed.. Nutritional intakes were not different between groups. In the control, subjects continued catabolism resulted in peripheral muscle wasting and centripetal obesity with diminished truncal LBM. The treatment group had improvement in lean body mass (P =.004) and bone mass (P =.025). The treatment group also had less peripheral muscle wasting with overall increases in upper/lower extremity LBM (P =.005). Hospital length of stay in days per percent of total body surface area burned was decreased in the insulin group (control = 1.03 +/- 0.1 vs 0.7 +/- 0.9 for insulin patients; P <.05).. Euglycemic hyperinsulinemia throughout the hospital course mitigates muscle catabolism and preserves lean body mass.

Topics: Adult; Blood Glucose; Body Composition; Body Weight; Burns; Calorimetry, Indirect; Child; Child, Preschool; Electrolytes; Energy Metabolism; Female; Follow-Up Studies; Glucose Clamp Technique; Glycogen; Humans; Hyperinsulinism; Hypoglycemic Agents; Insulin; Male; Muscle, Skeletal; Nutrition Assessment; Prospective Studies

Intravenous (IV) resuscitation of burn patients has greatly improved outcomes and become a cornerstone of modern burn care. However, the heavy fluids and vascular access required may not be feasible in austere environments, mass casualty, or delayed transport scenarios. Enteral resuscitation has been proposed for these situations; we sought to examine the effectiveness of this strategy on improving burn-induced kidney injury. Anesthetized Yorkshire swine sustaining 40% TBSA full-thickness contact burns were randomized to three groups (n = 6/group): fluid deprivation, ad libitum water access, or 70 mL/kg/d Oral Rehydration Salt solution (ORS). Urine and blood were collected at baseline (BL), 6, 12, 24, 32, and 48h post-burn, at which point tissue was harvested and CT angiography performed. Although fluid consumption by ad libitum and ORS groups were matched (132±54mL/kg versus 120±24mL/kg, respectively), ORS intake increased urine output compared with water and no water (47.3±9.0 mL/kg versus 16.1±2.5 mL/kg, and 24.5±1.7 mL/kg respectively). Plasma creatinine peaked 6h following burn (1.67±0.07mg/dL) in all animals, but at 48h was comparable to BL in animals receiving water (1.23±0.06mg/dL) and ORS (1.30±0.09mg/dL), but not fluid deprived animals (1.56±0.05mg/dL) (P<0.05). Circulating levels of blood urea nitrogen steadily increased, but also decreased by 48h in animals receiving enteral fluids (P<0.05). Water deprivation reduced renal artery diameter (-1.4±0.17mm), whereas resuscitation with water (-0.44±0.14 mm) or ORS maintained it (-0.63±0.20 mm;P< 0.02). Circulating cytokines IL-1β, IL-6, IFNγ, and GM-CSF were moderately elevated in the fluid-deprived group. Taken together, the data suggest that enteral resuscitation with ORS rescues kidney function following burn injury. Incorporating enteral fluids may improve outcomes in resource-poor environments and possibly reduce IV fluid requirements to prevent co-morbidities associated with over-resuscitation. Studies into different volumes/types of enteral fluids are warranted. While ORS has saved many lives in cholera-associated dehydration, it should be investigated further for use in burn patients.

Topics: Acute Kidney Injury; Animals; Burns; Disease Models, Animal; Enteral Nutrition; Female; Fluid Therapy; Glycogen; Kidney; Rehydration Solutions; Renal Artery; Swine; Vasoconstriction

Liver metabolism is altered after systemic injuries such as burns and trauma. These changes have been elucidated in rat models of experimental burn injury where the liver was isolated and perfused ex vivo. Because these studies were performed in fasted animals to deplete glycogen stores, thus simplifying quantification of gluconeogenesis, these observations reflect the combined impact of fasting and injury on liver metabolism. Herein we asked whether the metabolic response to experimental burn injury is different in fed vs. fasted animals. Rats were subjected to a cutaneous burn covering 20% of the total body surface area, or to similar procedures without administering the burn, hence a sham-burn. Half of the animals in the burn and sham-burn groups were fasted starting on postburn day 3, and the others allowed to continue ad libitum. On postburn day 4, livers were isolated and perfused for 1 hour in physiological medium supplemented with 10% hematocrit red blood cells. The uptake/release rates of major carbon and nitrogen sources, oxygen, and carbon dioxide were measured during the perfusion and the data fed into a mass balance model to estimate intracellular fluxes. The data show that in fed animals, injury increased glucose output mainly from glycogen breakdown and minimally impacted amino acid metabolism. In fasted animals, injury did not increase glucose output but increased urea production and the uptake of several amino acids, namely glutamine, arginine, glycine, and methionine. Furthermore, sham-burn animals responded to fasting by triggering gluconeogenesis from lactate; however, in burned animals the preferred gluconeogenic substrate was amino acids. Taken together, these results suggest that the fed state prevents the burn-induced increase in hepatic amino acid utilization for gluconeogenesis. The role of glycogen stores and means to increase and/or maintain internal sources of glucose to prevent increased hepatic amino acid utilization warrant further studies.

Topics: Amino Acids; Animals; Body Surface Area; Burns; Fasting; Glucose; Glycogen; Liver; Male; Nitrogen; Rats; Rats, Sprague-Dawley

The skin, the body's largest organ, plays an important role in the biotransformation/detoxification and elimination of xenobiotics and endogenous toxic substances, but its role in oxidative stress and insulin resistance is unclear. We investigated the relationship between skin detoxification and oxidative stress/insulin resistance by examining burn-induced changes in nicotinamide degradation. Rats were divided into four groups: sham-operated, sham-nicotinamide, burn, and burn-nicotinamide. Rats received an intraperitoneal glucose injection (2 g/kg) with (sham-nicotinamide and burn-nicotinamide groups) or without (sham-operated and burn groups) coadministration of nicotinamide (100 mg/kg). The results showed that the mRNA of all detoxification-related enzymes tested was detected in sham-operated skin but not in burned skin. The clearance of nicotinamide and N(1)-methylnicotinamide in burned rats was significantly decreased compared with that in sham-operated rats. After glucose loading, burn group showed significantly higher plasma insulin levels with a lower muscle glycogen level than that of sham-operated and sham-nicotinamide groups, although there were no significant differences in blood glucose levels over time between groups. More profound changes in plasma H(2)O(2) and insulin levels were observed in burn-nicotinamide group. It may be concluded that decreased skin detoxification may increase the risk for oxidative stress and insulin resistance.

Topics: Animals; Antioxidants; Blood Glucose; Burns; Glycogen; Hydrogen Peroxide; Insulin; Insulin Resistance; Male; Niacinamide; Oxidative Stress; Rats; Rats, Sprague-Dawley; Skin; Xenobiotics

Topics: Adrenergic beta-Antagonists; Burns; Dietary Carbohydrates; Energy Intake; Energy Metabolism; Glycogen; Humans; Muscle Proteins; Muscle, Skeletal; Propranolol

Complement activation is an important step for triggering of acute inflammatory reactions. Soluble human recombinant complement receptor type 1 (sCR1) blocks complement activation by both classical and alternative pathways. In addition to glycogen-induced peritonitis, three models of complement-dependent acute inflammatory injury have been used to assess the protective effects of sCR1: lung and dermal injury after intraalveolar or intradermal deposition of IgG immune complexes; acute lung injury resulting from intravascular activation of complement after the i.v. injection of cobra venom factor; and acute skin and lung injury (at 4 h) after thermal trauma involving 25 to 30% total body surface area. Vascular injury was quantified by increases in vascular permeability, hemorrhage, neutrophil infiltration, and, as indicated, tissue water content. Intravenous infusion of sCR1 reduced lung and dermal vascular injury in all models studied. In glycogen-induced peritoneal exudates sCR1-reduced neutrophil accumulation by 79%. In animals undergoing IgG immune complex-induced alveolitis, sCR1 treatment reduced vascular permeability and hemorrhage by 72 and 71%, respectively, and tissue accumulation of neutrophils was reduced by 68%. After cobra venom factor injection, sCR1 reduced increases in lung vascular permeability by 67%, hemorrhage by 73%, and lung myeloperoxidase content by 55%. Four hours after thermal injury of skin, sCR1-treated animals demonstrated significant protection against lung injury; increases in vascular permeability and hemorrhage were reduced by 45 and 46%, respectively, and myeloperoxidase content was lowered by 39%. In thermal injury of the skin, sCR1 injection reduced dermal vascular permeability by 25% at 1 h (p = NS) and 44% at 4 h. Water content in skin biopsies was also decreased. There was a dose-response relationship between the amount of sCR1 infused and the extent of protection in each of the injury models. These data demonstrate that sCR1 offers significant protection against complement-dependent tissue injury in the animal models studied and that the protective effects are related to reduced neutrophil content.

Topics: Animals; Antigen-Antibody Complex; Burns; Complement System Proteins; Elapid Venoms; Glycogen; Lung; Male; Neutrophils; Peroxidase; Rabbits; Rats; Rats, Inbred Strains; Receptors, Complement; Receptors, Complement 3b; Recombinant Proteins

Negative nitrogen balance and increased oxygen consumption after thermal injury in humans and experimental animals is related to the extent of the burn. To determine whether defective muscle metabolism is restricted to the region of injury, we studied protein and glucose metabolism in forelimb muscles of rats 48 h after a scalding injury of their hindquarters. This injury increased muscle protein degradation (PD) from 140 +/- 5 to 225 +/- 5 nmol tyrosine/g per h, but did not alter protein synthesis. Muscle lactate release was increased greater than 70%, even though plasma catecholamines and muscle cyclic AMP were not increased. Insulin dose-response studies revealed that the burn decreased the responsiveness of muscle glycogen synthesis to insulin but did not alter its sensitivity to insulin. Rates of net glycolysis and glucose oxidation were increased and substrate cycling of fructose-6-phosphate was decreased at all levels of insulin. The burn-induced increase in protein and glucose catabolism was not mediated by adrenal hormones, since they persisted despite adrenalectomy. Muscle PGE2 production was not increased by the burn and inhibition of prostaglandin synthesis by indomethacin did not inhibit proteolysis. The increase in PD required lysosomal proteolysis, since inhibition of cathepsin B with EP475 reduced PD. Insulin reduced PD 20% and the effects of EP475 and insulin were additive, reducing PD 41%. An inhibitor of muscle PD, alpha-ketoisocaproate, reduced burn-induced proteolysis 28% and lactate release 56%. The rate of PD in muscle of burned and unburned rats was correlated with the percentage of glucose uptake that was directed into lactate production (r = +0.82, P less than 0.01). Thus, a major thermal injury causes hypercatabolism of protein and glucose in muscle that is distant from the injury, and these responses may be linked to a single metabolic defect.

Topics: Adrenalectomy; Animals; Blood Chemical Analysis; Burns; Carbon Radioisotopes; Dexamethasone; Glycogen; Glycolysis; Hormones; Kinetics; Male; Muscles; Protein Biosynthesis; Proteins; Rats; Rats, Inbred Strains; Tritium

Topics: Adipose Tissue; Burns; Energy Intake; Enteral Nutrition; Glycogen; Humans; Infection Control; Parenteral Nutrition; Parenteral Nutrition, Total; Resuscitation; Wounds and Injuries

A toxic extent has been isolated and partially purified from burnt human and mouse skin and also from sera of severely burnt patients, which causes disturbances of energy metabolism and decreased synthesis rates for glucose and urea in the perfused rat liver. Enzymatically isolated hepatocytes from rat livers were used to study the toxic effects on hormonal sensitivity, synthetic functions and ultrastructure of the cells. A decreased synthesis of urea and glycogen was found in cells from rats treated 5 days before with "toxin" and in cells, which were directly incubated with the toxic factor. Glucagon increased urea synthesis in normal cells by 33%, and a decrease of 25% was caused by insulin. Cells of rats treated with the nontoxic precursor of the toxic factor from normal skin were similar, while those treated with "toxin" produced less urea and did not react to glucagon or insulin. Glycogen synthesis was reduced in cells directly incubated with the "toxin", however, the hormonal effects were still observed. Surface alterations of "toxin" treated cells and cells of "toxin" treated rats were found by scanning electronmicroscopy. These findings provide evidence of a direct cytotoxic effect of the toxic factor from burnt skin. It is proposed that the "toxin" acts on the cellular membrane with destruction of surface and receptorproteins.

Topics: Animals; Burns; Epinephrine; Female; Glucagon; Glycogen; Humans; Insulin; Liver; Mice; Microscopy, Electron, Scanning; Pancreatic Hormones; Rats; Skin; Toxins, Biological; Urea

Topics: Animals; Burns; Glucose; Glycogen; Hindlimb; Insulin; Lactates; Lactic Acid; Male; Muscles; Rats; Rats, Inbred Strains; Wound Healing

Topics: Adenosine Triphosphate; Animals; Burns; Glucose; Glycogen; Hindlimb; Insulin; Insulin Resistance; Male; Muscles; Rats; Rats, Inbred Strains; Time Factors

Modern intensive care combined with current improvements in the specific, systemic and local therapy of burns has delayed the mortal effects of severe burns. Nor has there been any significant improvement in this mortality during the last decade. The occurrence of uncontrollable infection and sepsis due to gram-negative bacteria or fungi as the basic cause of death was not a satisfactory explanation. So, progress should only be expected from a new concept in burn treatment. This new concept should be to view the burn disease as being caused by toxic factors induced by thermal injury to the skin. Electron-microscope studies in mice and rats have revealed similar mitochondrial alterations in hepatocytes after either a sublethal controlled burn injury or an intraperitoneal application of an equivalent dose, of a cutaneous burn toxin. The intraperitoneal injection of different amounts of the burn toxin indicated, that the extent of the mitochondrial changes correlated directly with the dose of toxin. Investigations of liver metabolism suggested an inhibition of the oxygenation chain. The incubation of isolated liver cells together with the burn toxin demonstrated by scanning electron microscopy a direct cytotoxic effect of the burn toxin. In animal tests the pathogenic effect of the burn toxin could be prevented by treatment with an antitoxic IgG generated in sheep. The fatal sepsis of severely burned patients is the consequence of a decreased host defence against infections, which is caused by a primary and general toxic alteration of the whole organism. One important aspect of treatment should therefore be the elimination of burn toxins. To achieve this management should include primary excision of the burns, local application of nonabsorbable protein-complex-binding substances and specific passive immunotherapy with an antitoxic IgG.

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Amino Acids; Animals; Burns; Glucose; Glycogen; Humans; Immunoglobulin G; Lactates; Liver; Mice; Rats; Skin; Toxins, Biological; Urea

Topics: Acid Phosphatase; Acute Disease; Adolescent; Adult; Aged; Alkaline Phosphatase; Blood Cell Count; Blood Proteins; Blood Transfusion; Bone Marrow; Burns; Child; Child, Preschool; Critical Care; Enzyme Activation; Glycogen; Hematopoiesis; Humans; Infant; Middle Aged

Acute insulin resistance developed after scald injury in the mouse. After 2h plasma glucose and insulin concentrations were each raised about two-fold. Glucose metabolism was studied in vitro in soleus muscles isolated at this time. Glycolysis and glycogen synthesis, and their stimulation by insulin, were unchanged in muscles from scalded mice, and insulin-stimulated transport of 2-deoxyglucose slightly increased, showing that the insulin resistance seen in vivo is not maintained in isolated tissues. Binding of insulin to liver cell membranes prepared from scalded mice was unaltered, whilst that of glucagon was slightly but significantly reduced, showing that changes in polypeptide-hormone receptors can occur within this short time. It was concluded that the acute loss of sensitivity to insulin after injury does not result from a change in insulin receptor sites and presumably reflects an impairment of glucose metabolism in vivo mediated by circulating hormones.

Topics: Animals; Biological Transport; Burns; Cell Membrane; Deoxyglucose; Glucose; Glycogen; Glycolysis; Insulin Resistance; Liver; Male; Mice; Muscles; Receptor, Insulin

The glycogen storage in rat skeletal muscle is reduced after a 20% third degree burn. The reason is probably a relative deficiency of insulin caused by insulin resistance at the tissue level. Posttraumatically increased sympatho-adrenal function has been suspected to cause this insulin resistance. In an earlier study, however, it has been shown that adrenal demedullation has no effect on the glycogen storage. In the present investigation an attempt was made to assess the importance of the increased peripheric sympathetic activity. Muscle glycogen, serum insulin and blood glucose were determined at the end of a glucose infusion after infliction of a burn both in 6-hydroxy-dopamine treated rats and rats with an intact peripheric sympathetic nervous system. It was found that a chemical sympathectomy did not improve the glycogen storage. The result indicates that the increased activity of the sympatho-adrenal system after a burn is not the main cause of the reduced skeletal muscle glycogen storage.

Topics: Animals; Burns; Glycogen; Insulin; Insulin Resistance; Male; Muscle, Skeletal; Rats; Rats, Sprague-Dawley; Sympathectomy, Chemical

The basal serum insulin level, insulin response and glycogen storage in the liver and skeletal muscle during a glucose infusion were studied 20-24 hours after experimental infliction of a burn in the rat. As was found in earlier studies, the liver glycogen storage was normal, while the storage of glycogen in the muscle was markedly inhibited. This inhibition cannot have been due to an absolute insuline deficiency, which has been discussed, as both the basal fasting level of insulin and the insulin response to glucose infusion were normal after the burn.

Topics: Animals; Blood Glucose; Burns; Fasting; Glucose; Glycogen; Infusions, Parenteral; Insulin; Insulin Secretion; Islets of Langerhans; Liver Glycogen; Male; Muscles; Rats

The glycogen synthetase activity and glycogen concentration were studied in rat skeletal muscle 24 hours after infliction of a burn. The active I-form of the enzyme was reduced. The total synthetase activity was unchanged. Expressed as a percentage of total synthetase activity, the I-form was decreased from 43.4% in control rats to 27.6% in burned rats. The fasting concentrations of serum insulin and muscle glycogen were not altered by the burn. The reduced synthetase I-form may explain the reduced glycogen storage capacity, demonstrated previously after a similar burn.

Topics: Animals; Burns; Glycogen; Glycogen Synthase; Insulin; Male; Muscles; Pelvis; Rats

The storage of glycogen in skeletal muscle and the liver was investigated after a 20% third-degree burn in the rat. The glycogen storage was studied 30 min and 20 hours post-burn. Thirty minutes after infliction of the burn the storage in the liver was 80% and in the muscle 60% of that in the control animals, and 20 hours after the burn 80% and 40%, respectively. Administration of insulin improved the storage in the muscle considerably--from 60% to 90% of the normal in the 30-minute group and from 40% to 75% in the 20-hour group. It was uncertain, on the other hand, whether insulin affected the glycogen storage in the liver. Possible causes of the reduced glycogen storage are discussed, including absolute or relative insulin deficiency.

Topics: Animals; Blood Glucose; Burns; Depression, Chemical; Glucose; Glycogen; Insulin; Liver Glycogen; Male; Muscles; Rats

In association with trauma the storage of glycogen, especially in skeletal muscle, is reduced. An increased release of adrenalin may be one of the causes of this phenomenon. In this study the effect of exogenously supplied adrenalin (0.5 mug/kg/min) on the storage of glycogen in the liver and skeletal muscle during a standardized infusion of glucose was studied in rats. A significant reduction of the glycogen storage in the liver was recorded. In the muscle the glycogen storage was practically eliminated. Simultaneous determinations of the serum insulin concentration showed very low insulin levels on administration of adrenalin, indicating a blockade of the insulin release in the beta-cells. When insulin was given at the same time the glycogen storage was almost completely normalized. This suggests that the deficiency of circulating insulin occurring on administration of adrenalin may be responsible for the lack of glycogen storage in the muscle.

Topics: Animals; Blood Glucose; Burns; Depression, Chemical; Drug Interactions; Epinephrine; Glucose; Glycogen; Insulin; Liver Glycogen; Male; Muscles; Rats; Stimulation, Chemical

Glycogen synthesis is reduced following trauma, especially in skeletal muscle. The author has shown previously that after an experimentally inflicted burn in the rat the glycogen storage in skeletal muscle is about 40% of the normal. In the present study an attempt was made to assess the importance of the endogenous adrenalin production in the adrenal medulla for this reduction in glycogen storage. With this aim the glycogen storage in the liver and skeletal muscle during a standardized glucose infusion was studied 20 hours after infliction of a burn both in rats with intact adrenal glands and in rats subjected to adrenal demedullation. In the muscle the glycogen storage was reduced in both groups, and to the same extent. In the liver no change in glycogen storage was recorded for either group. The results indicate that the catecholamines produced in the adrenal medulla, i.e. mainly adrenalin, are not the only cause of the reduced glycogen storage in skeletal muscle after trauma.

Topics: Adrenal Glands; Adrenal Medulla; Animals; Burns; Catecholamines; Glycogen; Liver Glycogen; Male; Muscles; Pelvis; Rats

Topics: Acid Phosphatase; Adrenal Glands; Alkaline Phosphatase; Animals; Ascorbic Acid; Blood Glucose; Blood Proteins; Burns; Flavonoids; Glycogen; Guinea Pigs; Hydrolyzable Tannins; L-Lactate Dehydrogenase; Liver; Muscles; Nucleic Acids; Pyruvates; Succinate Dehydrogenase; Tannins; Time Factors

Topics: Alkaline Phosphatase; Burns; Glycogen; Humans; Neutrophils; Phagocytosis

Topics: Adenosine Triphosphate; Animals; Ascorbic Acid; Burns; Carbohydrate Metabolism; Dermatologic Agents; Glycogen; Liver; Muscles; Phosphorus; Pyruvates; Rats; Steam; Tannins; Time Factors

Topics: Acetoacetates; Acetyl Coenzyme A; Animals; Blood Glucose; Burns; Carbon Radioisotopes; Fatty Acids, Nonesterified; Glutamates; Glycogen; Hindlimb; Hydroxybutyrates; Ischemia; Lactates; Liver; Mitochondria, Liver; Pyruvates; Rats; Wounds and Injuries

Topics: Adolescent; Adult; Age Factors; Aged; Burns; Child; Child, Preschool; Cicatrix; Citrates; Collagen; Female; Glycogen; Glycoproteins; Hexosamines; Hexoses; Humans; Hydroxyproline; Male; Methods; Middle Aged; Neuraminic Acids; Skin; Uronic Acids; Wound Healing

Topics: Adenosine Triphosphate; Animals; Burns; Glucose; Glycogen; Guinea Pigs; Lactates; Oxygen Consumption

1. The concentrations of several intracellular enzymes in rabbit skin have been measured 5 min, 2, 6 and 24 h after thermal injury.2. At 5 min and 2 h after a burn (60 degrees C for 1 min) there was a significant fall in the enzyme activities whereas at 6 h their activities were higher than control.3. It appears that the increase in enzyme concentrations in the lymph during the first few hours after thermal injury is associated with a fall in the enzyme concentrations in the tissues and therefore might be the result of leakage of enzyme from storage sites in the injured cells.4. The second increase in enzyme concentrations in the lymph which has been observed 6-18 h after thermal injury occurs at a time when there is also an increase in the enzyme concentrations in the tissue.5. It seems unlikely that these increased activities are due to new synthesis since there was no apparent correlation between tissue enzyme concentrations and protein synthetic activity, and the changes still occurred after administration of cycloheximide.6. There was a change in the LDH isoenzyme pattern after injury towards a predominance of LDH-1. This change did not occur immediately after the burn, but was present at 2 and 6 h, and returned to normal 24 h later.

Topics: Acid Phosphatase; Amino Acids; Animals; Burns; Cathepsins; Creatine Kinase; Cycloheximide; Glucuronidase; Glycogen; Isoenzymes; L-Lactate Dehydrogenase; Protein Biosynthesis; Rabbits; Ribosomes; Skin

Topics: Animals; Anterior Chamber; Burns; Cell Movement; Female; Fibroblasts; Glycogen; Guinea Pigs; Lipids; Male; Microscopy, Electron; Mitochondria, Muscle; Mitosis; Muscle, Smooth; Nerve Regeneration; Regeneration; Transplantation, Autologous; Transplantation, Homologous; Ureter; Urinary Bladder; Vas Deferens; Wound Healing

Topics: Acid Phosphatase; Amino Acids; Animals; Burns; Cats; Cycloheximide; Dactinomycin; DNA; Freezing; Glucuronidase; Glycogen; Hindlimb; Isoenzymes; L-Lactate Dehydrogenase; Lymph; Lysosomes; Muscles; Protein Biosynthesis; Skin; Transaminases

Topics: Animals; Blast Injuries; Blood Vessels; Burns; Coal; Dogs; Dust; Explosions; Gastric Mucosa; Glycogen; Hemorrhage; Hemostasis; Histocytochemistry; Inflammation; Intestinal Mucosa; Kidney; Liver; Liver Circulation; Liver Glycogen; Lung; Methane; Methods; Myocardium; Pulmonary Circulation; Regeneration

Topics: 4-Aminobenzoic Acid; Adrenal Cortex Hormones; Adrenal Glands; Aminobenzoates; Ascorbic Acid; Blood Chemical Analysis; Burns; Citrates; Dihydroergotoxine; Ergot Alkaloids; Glycogen; Histamine H1 Antagonists; Histocytochemistry; Ketoglutaric Acids; Lactates; Lipids; Liver; Metabolism; Muscles; Pharmacology; Pyruvates; Rats; Wound Healing

Topics: Alcohol Oxidoreductases; Animals; Burns; Glycogen; Guinea Pigs; Histocytochemistry; In Vitro Techniques; Phosphotransferases; Skin; Uracil Nucleotides; Wound Healing

Topics: Animals; Burns; Glycogen; Glycogenolysis; Rats

Topics: Burns; DNA; Glycogen; Histocytochemistry; Humans; Nucleic Acids; RNA; Skin

Topics: Animals; Burns; Glycogen; Heart; Histamine; Histamine Agents; Hypoxia; Myocardium; Rats

Topics: Burns; Desoxycorticosterone; Glucosides; Glycogen; Myocardium; Soft Tissue Injuries

Topics: Animals; Burns; Glycogen; Heart; Histamine; Rats; Skin Diseases; Soft Tissue Injuries

Topics: Animals; Burns; Glycogen; Liver; Rats; Shock