glycogen and Hypothermia

In the second part of this two part article the neonatal energy triangle elements of hypoxia and hypothermia are explored and the physiology of the first few hours of neonatal life drawn together into an integrated whole. This framework can assist in understanding the three most common difficulties encountered by the preterm baby and directing integrated and holistic care.

Topics: Adaptation, Physiological; Blood Glucose; Body Temperature Regulation; Glycogen; Holistic Health; Homeostasis; Humans; Hypoglycemia; Hypothermia; Hypoxia; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Neonatal Nursing; Oxygen Consumption; Respiratory Physiological Phenomena; Risk Factors; Work of Breathing

1. The presence of substrate cycles in tissues has been demonstrated by direct isotope methods in recent years. This demonstration has provided the impetus for a reappraisal of the roles of substrate cycling in metabolic regulation and in heat production. These aspects of substrate cycling are discussed in this paper. The relationship between near-equilibrium reactions and substrate cycles is emphasized, since this provides a basis for the derivation of a function describing in precise quantitative terms the factors governing the amplification provided by substrate cycles in metabolic regulation. Some examples of the roles of substrate cycles in providing sensitivity in metabolic regulation are described. The importance of substrate cycling in heat generation in the flight muscle of the bumble-bee and in brown adipose tissue is discussed in detail. 2. We point out that the two possible roles of cycling, heat production and amplification, are intimately linked so that they must be discussed together. It is proposed that variable rates of substrate cycling may be possible so that, for short periods of time. sensitivity can be maximal without excessive heat generation. Variable rates over the long term may be involved in weight control, and the control of such variability in cycling rates may be impaired in obese subjects. Finally, the possibilities that substrate cycles provide explanations for the specific dynamic action of food and for alcoholic and accidental hypothermia are raised.

Topics: Adipose Tissue; Aged; Allosteric Regulation; Animals; Blood Glucose; Body Temperature Regulation; Citric Acid Cycle; Energy Metabolism; Epinephrine; Ethanol; Fatty Acids; Feedback; Fructosephosphates; Glucosephosphates; Glycogen; Humans; Hypothermia; Insecta; Kidney; Liver; Metabolism; Mitochondria; Models, Biological; Muscles; NAD; Rats; Sodium; Triglycerides

Topics: Adenosine Triphosphate; Animals; Cell Nucleus; Citrates; Coronary Disease; Disease Models, Animal; Dogs; Endoplasmic Reticulum; Glycogen; Heart Arrest; Hypothermia; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Phosphates; Phosphocreatine; Potassium; Potassium Chloride; Procaine; Rats

Armanni-Ebstein lesions were first described by Luciano Armanni, a pathologist at the University of Naples, during autopsy studies undertaken in 1872, as a unique vacuolar nephropathy associated with poorly controlled diabetes that involves selective renal epithelial cell glycogen accumulation. However, within the last two decades, a broader range of vacuolar changes, including lipid deposition, have also been termed Armanni-Ebstein (AE) lesions, creating some confusion on possible etiology. We would suggest that the term AE phenomenon would be best reserved for the original clear cell change associated with glycogen deposition, and that this should be clearly distinguished from subnuclear lipid vacuolization ("basal vacuolization"). Although there is obvious inter-relation between these two types of vacuoles, they appear morphologically and biochemically distinct from each other. More precise classification may assist in clarifying the causal processes and possible diagnostic significance of different types of renal epithelial vacuolization at autopsy.

Topics: Animals; Epithelial Cells; Forensic Pathology; Glycogen; Humans; Hypothermia; Ketosis; Kidney Tubules; Lipids; Terminology as Topic; Vacuoles

Mechanism of rhodiola root extract adaptogenic activity was studied in rats. The extract was orally administered in rats (100mg/kg body weight), 30 min prior to cold (5 degrees C)-hypoxia (428 mmHg)-restraint (C-H-R) exposure up to fall of T(rec)23 degrees C and recovery (T(rec)37 degrees C) from hypothermia. In untreated control rats serum lactate and non-esterified fatty acids (NEFA) increased on attaining T(rec)23 degrees C with decreased blood enzyme activities hexokinase (HK), phosphofructokinase (PFK), citrate synthase (CS) and glucose-6-phosphate dehydrogenase (G-6-PD), on attaining T(rec)23 degrees C and T(rec)37 degrees C. Decreases were also observed in liver and muscle tissues HK and G-6-PD enzyme activities and liver glycogen and CS on attaining T(rec)23 degrees C and recovery; muscle PFK during recovery; muscle CS on attaining T(rec)23 degrees C. Single and five doses of extract administration restricted increase in serum lactate values of rats on attaining T(rec)23 degrees C and maintained blood NEFA in single dose extract treated animals, indicating improved utilization of NEFA as energy fuel. The single and five doses extract treatment decreased or better maintained tissue glycogen and enzyme activities, viz. HK, PFK, CS and G-6-PD, in blood, liver and muscle, on attaining T(rec)23 degrees C and recovery. The results suggest that rhodiola extract treatment in rats shifted anaerobic metabolism to aerobic, during C-H-R exposure and post stress recovery.

Topics: Animals; Blood Glucose; Cold Temperature; Energy Metabolism; Fatty Acids, Nonesterified; Glycogen; Glycolysis; Hypothermia; Hypoxia; Lactic Acid; Male; Plant Extracts; Plant Roots; Proteins; Rats; Rats, Sprague-Dawley; Restraint, Physical; Rhodiola; Stress, Psychological

Mice lacking acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), a key enzyme in triglyceride synthesis, have increased energy expenditure and therefore are resistant to obesity. Because ambient temperature can significantly affect energy expenditure in mice, we undertook these studies to determine the effects of different ambient temperatures on energy expenditure, food intake, and thermoregulation in DGAT1-deficient [Dgat1(-/-)] mice. Dgat1(-/-) mice had increased energy expenditure irrespective of changes in the ambient temperature. Although core temperature was normal, surface temperature was increased in Dgat1(-/-) mice, most likely reflecting an active mechanism to dissipate heat from increased thermogenesis. Dgat1(-/-) mice had increased food intake at baseline, and this hyperphagia became more pronounced upon exposure to cold. When fasted in a cold environment, Dgat1(-/-) mice developed hypothermia, which was associated with hypoglycemia. These results suggest that the hyperphagia in Dgat1(-/-) mice is a secondary mechanism that compensates for the increased utilization of fuel substrates. Our findings offer insights into the mechanisms of hyperphagia and increased energy expenditure in a murine model of obesity resistance.

Topics: Acyltransferases; Animals; Blood Glucose; Body Temperature; Body Temperature Regulation; Carrier Proteins; Cold Temperature; Diacylglycerol O-Acyltransferase; Eating; Energy Metabolism; Fasting; Female; Gene Expression; Glycogen; Hyperphagia; Hypoglycemia; Hypothermia; Ion Channels; Liver; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondrial Proteins; Muscle, Skeletal; Obesity; Temperature; Uncoupling Protein 1; Weight Loss

The neuroendocrine-specific protein 7B2, which serves as a molecular escort for proPC2 in the secretory pathway, promotes the production of enzymatically active PC2 and may have non-PC2 related endocrine roles. Mice null for 7B2 exhibit a lethal phenotype with a complex Cushing's-like pathology, which develops from intermediate lobe ACTH hypersecretion as a consequences of interruption of PC2-mediated peptide processing as well as undefined consequences of the loss of 7B2. In this study we investigated the endocrine and metabolic alterations of 7B2 null mice from pathological and biochemical points of view. Our results show that 7B2 nulls exhibit a multisystem disorder that includes severe pathoanatomical and histopathologic alterations of vital organs, including the heart and spleen but most notably the liver, in which massive steatosis and necrosis are observed. Metabolic derangements in glucose metabolism result in glycogen and fat deposition in liver under conditions of chronic hypoglycemia. Liver failure is also likely to contribute to abnormalities in blood coagulation and blood chemistry, such as lactic acidosis. A hypoglycemic crisis coupled with respiratory distress and intensive internal thrombosis most likely results in rapid deterioration and death of the 7B2 null.

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Cause of Death; Corticosterone; Cushing Syndrome; Glucagon; Glucose; Glycogen; Hormones; Hypothermia; Lactic Acid; Liver; Magnesium; Metyrapone; Mice; Mice, Knockout; Multiple Organ Failure; Nerve Tissue Proteins; Neuroendocrine Secretory Protein 7B2; Pituitary Hormones; Radioimmunoassay; Seizures; Tissue Distribution

Investigation of the mechanism of increased tolerance to stress induced hypothermia after the administration of composite Indian herbal preparation II (CIHP II), a combination of several plant ingredients and minerals.. The effect of oral CIHP II administration (1 mg/g of body weight), prior to cold (5 degrees C)-hypoxia (428 mm Hg)-restraint (C-H-R) exposure in rats on cardiac and skeletal muscle oxidation was studied in vitro by estimating conversion of glucose-U-14C and Palmitate-1-(14)C to 14CO2. In vitro adipose tissue lipolysis and incorporation of glucose-U-14C into skeletal muscle glycogen was also studied.. A single dose of CIHP II-enhanced resistance to hypothermia (rectal temperature [T(rec)] 23 degrees C) during C-H-R exposure as evidenced by increased glucose turnover rate in heart and skeletal muscle tissue. The blood glucose and skeletal muscle glycogen were conserved. Cardiac free fatty acid oxidation was also increased. During recovery from hypothermia (T(rec) 37 degrees C) blood glucose and muscle glycogen levels were conserved. Five doses of CIHP II increased resistance to cold by increased adipose fat mobilization and cardiac oxidation. Glucose oxidation was spared. During recovery from hypothermia, the glucose turnover and oxidation in skeletal muscle was increased as was fat mobilization from adipose tissue and its oxidation by heart muscle.. CIHP II intake prior to C-H-R exposure resulted in increased glucose turnover rate and fat utilization. This perhaps helped increase the resistance to C-H-R-induced hypothermia and speeded recovery.

Topics: Animals; Blood Glucose; Glycogen; Hypothermia; Immune Tolerance; Medicine, Ayurvedic; Muscle, Skeletal; Phytotherapy; Plant Extracts; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Stress, Physiological

In the present study we examined the impact of glycolysis and glucose oxidation on myocardial calcium control and mechanical function of fatty acid-perfused rat hearts subjected to hypothermia rewarming. One group (control) was given glucose (11.1 mM) and palmitate (1.2 mM) as energy substrates. In a second group glycolysis was inhibited by iodoacetate (IAA, 100 microM) and replacement of glucose with pyruvate (5 mM), whereas in the third group glucose oxidation was stimulated by administration of dichloroacetate (DCA, 1 mM) and insulin (500 microU/ml). All groups showed a rise in myocardial calcium ([Ca]total in response to hypothermia (10 degrees C). However, [Ca]total was significantly lower both in IAA- and DCA-treated hearts, as compared to controls (2.20 +/- 0.22 and 2.94 +/- 0.20 v 3.83 +/- 0.29 nmol/mg dry wt., P < 0.025). The reduced calcium load in the treated hearts was correlated with higher levels of high energy phosphates. Following rewarming control and DCA-treated hearts still showed elevated [Ca]total, whereas IAA-treated hearts [Ca]total was not different from the pre-hypothermic value. All groups showed a reduction in cardiac output following rewarming. Furthermore, the control group, in contrast to both IAA- and DCA-treated hearts, showed a significant reduction in systolic pressure. These results show that hypothermia-induced calcium uptake in glucose and fatty acid-perfused rat hearts was reduced by two different metabolic approaches: (1) inhibition of glycolysis by IAA while simultaneously by-passing the glycolytic pathway by exogenous pyruvate: and (2) stimulation of glucose oxidation by DCA. Thus, glycolytic ATP is not an essential regulator of sarcolemmal calcium transport under the present experimental conditions. Instead, we suggest that a change in oxidative substrate utilization in favour of carbohydrates may improve myocardial calcium homeostasis during hypothermia and rewarming.

Topics: Adenosine Triphosphate; Animals; Calcium; Carbohydrate Metabolism; Cardiac Output; Fatty Acids; Glucose; Glycogen; Hypothermia; Lactic Acid; Male; Myocardial Reperfusion; Myocardium; Oxidation-Reduction; Perfusion; Phosphocreatine; Rats; Rats, Sprague-Dawley

This study presents the use of physiological principles and assessment techniques in addressing four objectives that can enhance a swimmer's likelihood of successfully swimming the English Channel. The four objective were: (1) to prescribe training intensities and determine ideal swimming pace; (2) to determine the amount of insulation needed, relative to heat produced, to diminish the likelihood of the swimmer suffering from hypothermia; (3) to calculate the caloric expenditure for the swim and the necessary glucose replacement required to prevent glycogen depletion; and (4) to determine the rate of acclimatization to cold water (15.56 C/60 F).. The subject participated in several pool swimming data collection sessions including a tethered swim incremental protocol to determine peak oxygen consumption and onset of lactate accumulation and several steady state swims to determine ideal swimming pace at 4.0 mM/L of lactate. Additionally, these swims provided information on oxygen consumption, which in combination with ultrasound assessment of subcutaneous fat was used to assess heat production and insulation capabilities. Finally, the subject participated in 18 cold water immersions to document acclimatization rate.. The data demonstrated the high fitness level of this subject and indicated that at a stroke rate of 63 stokes/min, HR was 130 heats/min and lactate was 4 mM/L. At this swimming pace the swimmer would need to consume 470 kcal of glucose/hr. In addition, the energy produced at this swim pace was 13.25 kcal/min while the energy lost at the present subcutaneous fat quantity was 13.40 kcal/min, requiring a fat weight gain of 6,363.03 g (13.88 lbs) to resist heat loss.. Finally, the data from the cold water immersions suggested that acclimatization occurred following two weeks of immersions. There results were provided to the swimmer and utilized in making decisions in preparation for the swim.

Topics: Acclimatization; Adipose Tissue; Adult; Anaerobic Threshold; Body Mass Index; Body Temperature; Cold Temperature; Dietary Carbohydrates; Energy Intake; Energy Metabolism; Glucose; Glycogen; Humans; Hypothermia; Lactates; Male; Motor Activity; Oceans and Seas; Oxygen Consumption; Physical Endurance; Physical Fitness; Swimming; Weight Gain

The causality of vascular and parenchymal damage to the central nervous system (CNS) was examined in rats with thiamine deficiency. Male Sprague-Dawley rats were divided into two groups; one was given a thiamine-deficient diet (TDD) and injected intraperitoneally with 10 micrograms/100 g bodyweight pyrithiamine (PT) in order to analyze morphometrically the topographical and sequential relationship between vascular and parenchymal changes and vasodilatation, and the other was given a TDD and 50 micrograms/100 g bodyweight PT in order to determine hemorrhagic sites using serial sections. Histological examination showed that spongiotic change occurred selectively in the inferior colliculus (100%) from day 19, and thereafter in the thalamus (95%), mammillary body (50%) and nuclei olivaris and vestibularis of the pons (25%), with or without hemorrhage. Simultaneously, glycogen accumulation was also observed in these regions at a frequency similar to that of hemorrhage. Ultrastructurally, however, hydropic swelling of astrocytic and neuronal processes without glycogen accumulation was observed as early as day 9 in the inferior colliculus, at which time an increase of glial fibrillary acidic protein-positive processes was also recognized. The superior colliculus was completely spared. From day 22 vasodilatation of the inferior colliculus occurred, concomitantly with bodyweight loss and neurological symptoms. Twenty-two examined hemorrhages, which occurred in the thalamus and inferior colliculus, were distributed along the arterioles or capillaries on the arterial side. In conclusion, the morphological CNS changes caused by thiamine deficiency with administration of low-dose PT in rats begin as hydropic swelling of neuronal and astrocytic processes, followed by hemorrhage and, thereafter, by vasodilation. The predilection for hemorrhage on the arterial side without parenchymal changes suggests that petechial hemorrhage is not simply secondary to parenchymal changes, but is due to hemodynamic change resulting from thiamine deficiency-induced vascular dysfunction.

Topics: Animals; Antimetabolites; Ataxia; Body Weight; Brain; Cerebral Hemorrhage; Glial Fibrillary Acidic Protein; Glycogen; Hypothermia; Immunohistochemistry; Inferior Colliculi; Male; Mammillary Bodies; Pyrithiamine; Rats; Rats, Sprague-Dawley; Seizures; Thalamus; Thiamine Deficiency; Vasodilation; Wernicke Encephalopathy

An increased sensitivity of adrenalectomized (Adex) rats to intravenous (IV) injection of recombinant human tumor necrosis factor (rHuTNF) was manifested by a marked increase in the rate of mortality. The rats that died exhibited severe hypoglycemia and hypothermia. Administration of 2.5 or 10 micrograms/100 g body weight (3% or 12%) of the lethal dose in sham-operated rats (90 micrograms/100 g body weight) rHuTNF caused a mortality rate of 50% or 100%, respectively, within 4 hours of its injection. Pre-administration of dexamethasone or intermittent glucose infusion protected the animals from the lethal effect of rHuTNF. Indomethacin did not change the mortality rate in rHuTNF-treated Adex rats, but prevented it in sham-operated rats. The rats that died exhibited a marked decrease in body temperature, but only Adex rats developed hypoglycemia after low doses of TNF. Pretreatment with dexamethasone prevented the hypothermia in both Adex and sham-operated rats, while indomethacin was effective only in sham-operated rats and did not prevent the hypothermia or the hypoglycemia in Adex rats. In the surviving rHuTNF-treated Adex rats, a rapid increase in body temperature occurred, blood glucose decreased to 30 mg/dL, serum insulin concentration decreased to 6 microU/mL, liver glycogen content was reduced by 98%, and a significant reduction in liver phosphoeonolpyruvate carboxykinase (PEPCK) and liver microsomal glucose-6-phosphatase activities was observed. Repeated administration of glucose IV to rHuTNF-treated Adex rats caused an increase in blood glucose and insulin concentrations, and some repletion in liver glycogen content. Injection of rHuTNF, 2.5 to 10 micrograms/100 g body weight, to sham-operated rats caused a significant but slower increase in body temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenal Medulla; Adrenalectomy; Animals; Blood Glucose; Body Temperature Regulation; Dexamethasone; Glucose; Glucose-6-Phosphatase; Glycogen; Hypoglycemia; Hypothermia; Indomethacin; Lipoprotein Lipase; Male; Microsomes, Liver; Phosphoenolpyruvate Carboxykinase (GTP); Rats; Recombinant Proteins; Time Factors; Tumor Necrosis Factor-alpha

Regulation of glycolysis was assessed in winter- and summer-acclimatized goldfinches (Carduelis tristis). We exposed birds to a thermo-neutral temperature (30 degrees C), moderate cold (-15 degrees C), and severe cold (0 degrees C in an atmosphere of 21% O2-79% He), and then measured concentrations of glycogen, glycolytic intermediates, and citrate in the pectoralis muscles. Winter birds used less glycogen when exposed to moderate cold than did summer birds, confirming the carbohydrate sparing noted by Marsh and Dawson [Am. J. Physiol. 242 (Regulatory Integrative Comp. Physiol. 11): R563-R569, 1982]. However, depletion of muscle glycogen did not correlate with thermoregulatory failure in this study. Concentrations of glucose 6-phosphate and fructose 6-phosphate in the pectoralis muscles were approximately 1.9 and 0.3 mumol/g wet mass in birds exposed to thermoneutral temperatures. The levels of these intermediates fell 50-70% under conditions known to enhance flux through glycolysis as indicated by increased glucose turnover and glycogen depletion. This information identifies phosphofructokinase (PFK) as a major regulated step in glycolysis in these highly aerobic skeletal muscles. Winter birds maintained the inhibition of this step under conditions of moderate cold. However, concentrations of citrate, which have been hypothesized to be an important inhibitor of PFK, did not correlate with the observed pattern of inhibition. Therefore, if the enhanced beta-oxidative capacity of winter birds is important in the regulation of glycolysis, a mechanism other than the accumulation of citrate may be involved.

Topics: Acclimatization; Animals; Birds; Cold Temperature; Fructosephosphates; Glucose-6-Phosphate; Glucosephosphates; Glycogen; Glycolysis; Hypothermia; Oxygen Consumption; Pectoralis Muscles; Seasons

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.

Topics: Adult; Body Temperature; Body Temperature Regulation; Glycogen; Humans; Hypothermia; Male; Muscles; Physical Exertion; Time Factors

The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 degrees C) was produced by exposure to helox (80% helium:20% oxygen) at 0 +/- 1 degree C. Hyperglycemia was noted during the induction process (169 +/- 8 in control vs 326 +/- 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming (Tre of 33 +/- 1 degrees C) was reduced (153 +/- 16 mg/dl) significantly (P less than 0.05). Serum insulin was depressed during hypothermic induction (from 48 +/- 4 in controls to 19 +/- 3 microU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.

Topics: Animals; Arousal; Blood Glucose; Body Temperature; Glycogen; Hypothermia; Insulin; Insulin Secretion; Liver Glycogen; Male; Muscles; Myocardium; Rats; Rats, Inbred Strains

In the past three decades, wheelchair sports have become an international reality. Disabled athletes are exercising their right to accept the challenges and risks taken by able-bodied athletes. Marathon racing over a 26-mile, 385-yard course is the latest and most strenuous of the wheelchair athletic events. The small amount of available research data on wheelchair sports has been summarized, as well as some relevant data from exercise physiology studies on able-bodied subjects. Physicians and other health professionals who work with disabled people should be knowledgeable about the risks and benefits of wheelchair sports. Much more basic research is needed to improve the safety, training techniques, and performance of wheelchair athletes.

Topics: Athletic Injuries; Body Weight; Capillaries; Dehydration; Energy Metabolism; Female; Glycogen; Humans; Hypothermia; Male; Muscles; Oxygen Consumption; Paraplegia; Sports; Sports Medicine; Wheelchairs

Topics: Animals; Body Temperature; Brain; Brain Chemistry; Chickens; Dextroamphetamine; Female; Glycogen; Hypothermia; Male

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Animals; Brain; Catheterization; Cerebral Cortex; Cold Temperature; Electric Conductivity; Glucose; Glycogen; Hypothermia; Lactates; Perfusion; Phosphates; Phosphocreatine; Rabbits; Time Factors

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Cold Temperature; Creatine; Fatty Liver; Fructose-Bisphosphate Aldolase; Glycogen; Hair; Hematocrit; Hemorrhage; Hypothermia; Isoenzymes; Kidney; L-Lactate Dehydrogenase; Leukocyte Count; Lipids; Liver; Liver Glycogen; Lung Diseases; Male; Muscles; Myocardium; Necrosis; Phosphotransferases; Rabbits; Time Factors

Topics: Animals; Cell Membrane; Duodenum; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Hypothermia; Intestinal Mucosa; Male; Microscopy, Electron; Mitochondria; Mitochondrial Swelling; Radiation Injuries, Experimental; Rats; Time Factors

1. Physostigmine (0.1 mg/kg i.v.) given at 37 degrees C and 25 degrees C rectal temperatures, completely protected the hypothermic dog heart against ventricular fibrillation.2. Pentolinium, atropine, vagotomy and reserpine did not significantly alter the incidence of ventricular fibrillation.3. The incidence of ventricular fibrillation under hypothermia could be significantly increased by ligating the anterior descending branch of the left coronary artery. The incidence of ventricular fibrillation in coronary ligated hypothermic dogs was reduced to half by physostigmine pretreatment.4. Hypothermia produced ventricular glycogen depletion and physostigmine prevented ventricular glycogenolysis under hypothermia. However, in the normothermic state physostigmine itself produced a significant decrease in cardiac glycogen.5. The relation between the antifibrillatory and antiglycogenolytic effects of physostigmine under hypothermia are discussed.

Topics: Animals; Atropine; Blood Pressure; Coronary Vessels; Dogs; Glycogen; Heart Atria; Heart Rate; Heart Ventricles; Hypothermia; Ligation; Myocardium; Pentolinium Tartrate; Physostigmine; Reserpine; Statistics as Topic; Vagotomy; Ventricular Fibrillation

Topics: Adipose Tissue; Adipose Tissue, Brown; Animals; Blood Glucose; Body Temperature; Chlorpromazine; Desipramine; Fatty Acids, Nonesterified; Female; Glycogen; Hypothermia; Lactates; Liver Glycogen; Rats; Reserpine

Topics: Acid-Base Equilibrium; Adenosine Triphosphate; Animals; Brain; Brain Edema; Carbon Dioxide; Electrolytes; Extracorporeal Circulation; Glucose; Glycogen; Hydrogen-Ion Concentration; Hypothermia; Hypothermia, Induced; Hypoxia; Lactates; Male; Nucleosides; Partial Pressure; Phosphates; Phosphocreatine; Potassium; Pyruvates; Rats; Sodium; Water

Topics: Animals; Dogs; Glycogen; Histocytochemistry; Hypothermia; L-Lactate Dehydrogenase; Liver; Myocardium; Phosphoric Monoester Hydrolases; Succinate Dehydrogenase

Topics: Adrenocorticotropic Hormone; Animals; Cerebral Cortex; Chlorpromazine; Fever; Glucocorticoids; Glycogen; Hypothermia; Rats

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Body Temperature; Cerebral Cortex; Chlorpromazine; Fever; Glycogen; Hypothermia; Hypothermia, Induced; Rats; Triamcinolone Acetonide

Topics: Carbohydrate Metabolism; Carbon Isotopes; Fasting; Fatty Acids; Glucose; Glycogen; Hypothermia; Hypothermia, Induced; Hypoxia; Lactates; Lipid Metabolism; Myocardium; Palmitates; Palmitic Acid; Radiometry; Rats; Temperature

Topics: Adenosine Triphosphate; Animals; Coenzymes; Electrocardiography; Electron Transport Complex II; Glycogen; Histocytochemistry; Hypothermia; Hypothermia, Induced; Lactates; Metabolism; Myocardium; NAD; NADP; Oxidoreductases; Phosphocreatine; Pyruvates; Rats; Research; Rodentia; Sciuridae; Succinate Dehydrogenase

Topics: Animals; Animals, Newborn; Asphyxia Neonatorum; Biomedical Research; Cats; Chlorpromazine; Dogs; Glycogen; Guinea Pigs; Humans; Hypothermia; Hypothermia, Induced; Infant, Newborn; Infant, Premature; Metabolism; Myocardium; Rabbits; Research; Swine

Cardiac glycogen was not affected by cooling guinea pigs for short periods. In normothermic animals it was reduced 75 percent or more at the time of death from asphyxia. Quickly cooled animals asphyxiated until the time of death of warm controls showed no significant losses of cardiac glycogen; animals cooled while breathing 10 percent oxygen plus 5 percent carbon dioxide showed slight reductions. Therefore, hypothermia spares cardiac glycogen during asphyxia, but there are factors other than cardiac glycogen which influence survival of asphyxiated animals.

Topics: Animals; Asphyxia; Carbohydrate Metabolism; Carbon Dioxide; Glycogen; Guinea Pigs; Heart; Hypothermia; Hypothermia, Induced; Myocardium; Physiology; Research

Topics: Adrenalectomy; Animals; Carbohydrate Metabolism; Cricetinae; Glucose; Glycogen; Hypothermia; Hypothermia, Induced; Liver Glycogen; Metabolism; Muscles; Myocardium; Pharmacology; Positive-Pressure Respiration; Rats; Reptiles; Research; Tubocurarine; Turtles

Topics: Animals; Asphyxia; Blood Glucose; Brain; Glycogen; Heart; Heart, Artificial; Hypothermia; Hypothermia, Induced; Insulin; Iodine; Liver; Liver Glycogen; Myocardium; Prednisolone; Rabbits; Research

Topics: Glycogen; Hypothermia; Hypothermia, Induced; Muscles

Topics: Animals; Carbohydrate Metabolism; Glucose; Glycogen; Glycogenolysis; Hypothermia; Hypothermia, Induced; Lactates; Pyruvates; Rats

Topics: Glycogen; Glycogenolysis; Heart; Humans; Hypothermia; Hypothermia, Induced; Myocardium

Topics: Animals; Glycogen; Glycogenolysis; Hypothermia; Myocardium; Near Drowning; Oxygen Consumption; Rats; Rewarming

Topics: Brain; Glycogen; Humans; Hypothermia; Hypothermia, Induced; Liver; Muscle, Skeletal; Muscle, Striated

Topics: Animals; Glycogen; Glycogenolysis; Hypothermia; Myocardium; Phosphates; Rats

Topics: Body Temperature; Brain; Glycogen; Glycogenolysis; Heart; Hypothermia; Myocardium

Topics: Animals; Body Temperature; Glycogen; Glycogenolysis; Hypothermia; Liver; Muscles; Musculoskeletal Physiological Phenomena

Topics: Blood Glucose; Body Temperature; Glycogen; Hypothermia; Liver; Oxygen Consumption; Temperature