phosphocreatine and Fever

Plasma concentrations of procalcitonin (PCT) have been shown to be elevated in bacterial and fungal infections. In contrast to C-reactive protein (CRP), PCT is not elevated in inflammations of noninfectious origin. Febrile inflammatory conditions are frequent in patients with hemato-oncological diseases. A reliable marker to discriminate infectious inflammations from drug-related and tumor-associated fever is still lacking. To evaluate the impact of PCT in this setting, PCT and CRP were prospectively measured in 95 febrile hemato-oncological patients. Infections could be identified in 40 of 95 patients: 38 of 95 had fever of unknown origin (FUO), 9 patients were suspected to suffer from drug-related fever, and 8 patients from tumor-associated fever. In the noninfection group (drug-related and tumor-associated fever), PCT levels were significantly lower than in patients with infections (P<0.001) or FUO (P<0.001). Differences were still highly significant comparing patients with suspected drug-related or tumor-associated fever alone with the infection or the FUO cohort. All eight patients with tumor-associated fever as well as eight of the nine patients with drug-related fever had PCT levels within the normal range (<0.5 micro g/l). CRP values only partially allowed discrimination between the various subgroups. Differences were significant between patients with drug-related fever and the infection (P=0.001) or FUO group (P=0.004). However, as CRP levels were far above the normal range also in the patients with drug-related fever, the significance of individual values was rather limited. In conclusion, PCT may provide useful additional information to assess the clinical significance of febrile conditions. PCT may facilitate the decision on when to initiate antimicrobial or cytotoxic therapy.

Topics: Adolescent; Adult; Aged; Antineoplastic Agents; Biomarkers; Calcitonin; Calcitonin Gene-Related Peptide; Diagnosis, Differential; Female; Fever; Hematologic Neoplasms; Humans; Infections; Male; Middle Aged; Phosphocreatine; Protein Precursors; ROC Curve; Sensitivity and Specificity

1. The present study examined whether reductions in muscle blood flow with exercise-induced dehydration would reduce substrate delivery and metabolite and heat removal to and from active skeletal muscles during prolonged exercise in the heat. A second aim was to examine the effects of dehydration on fuel utilisation across the exercising leg and identify factors related to fatigue. 2. Seven cyclists performed two cycle ergometer exercise trials in the heat (35 C; 61 +/- 2 % of maximal oxygen consumption rate, VO2,max), separated by 1 week. During the first trial (dehydration, DE), they cycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive DE and hyperthermia (3.9 +/- 0.3 % body weight loss and 39.7 +/- 0.2 C oesophageal temperature, Toes). On the second trial (control), they cycled for the same period of time maintaining euhydration by ingesting fluids and stabilising Toes at 38.2 +/- 0.1 degrees C. 3. After 20 min of exercise in both trials, leg blood flow (LBF) and leg exchange of lactate, glucose, free fatty acids (FFA) and glycerol were similar. During the 20 to 135 +/- 4 min period of exercise, LBF declined significantly in DE but tended to increase in control. Therefore, after 120 and 135 +/- 4 min of DE, LBF was 0.6 +/- 0.2 and 1.0 +/- 0.3 l min-1 lower (P < 0.05), respectively, compared with control. 4. The lower LBF after 2 h in DE did not alter glucose or FFA delivery compared with control. However, DE resulted in lower (P < 0.05) net FFA uptake and higher (P < 0.05) muscle glycogen utilisation (45 %), muscle lactate accumulation (4.6-fold) and net lactate release (52 %), without altering net glycerol release or net glucose uptake. 5. In both trials, the mean convective heat transfer from the exercising legs to the body core ranged from 6.3 +/- 1.7 to 7.2 +/- 1.3 kJ min-1, thereby accounting for 35-40 % of the estimated rate of heat production ( approximately 18 kJ min-1). 6. At exhaustion in DE, blood lactate values were low whereas blood glucose and muscle glycogen levels were still high. Exhaustion coincided with high body temperature ( approximately 40 C). 7. In conclusion, the present results demonstrate that reductions in exercising muscle blood flow with dehydration do not impair either the delivery of glucose and FFA or the removal of lactate during moderately intense prolonged exercise in the heat. However, dehydration during exercise in the heat elevates carbohydrate oxidation and lactate pro

Topics: Adult; Blood Glucose; Body Temperature; Carbon Dioxide; Dehydration; Epinephrine; Exercise; Exercise Test; Fatigue; Fatty Acids, Nonesterified; Fever; Glucagon; Glycerol; Glycogen; Humans; Insulin; Lactic Acid; Male; Muscle, Skeletal; Oxygen Consumption; Phosphocreatine; Regional Blood Flow; Thermodynamics

We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced greater than or equal to 1 hour before ischemia and was maintained during 1.5-2 hours of recirculation in nine cats; four cats were subjected to hyperthermia without cerebral ischemia, six to hyperthermia during recirculation (after return of intracellular pH to preischemic values), and 14 to normothermic ischemia and recirculation. Our data indicate that preischemic hyperthermia results in an intracellular cerebral pH during recirculation significantly lower than that in normothermic cats. In hyperthermic cats beta-ATP and phosphocreatine (PCr) concentrations and the ratio of PCr to inorganic phosphate failed to return to preischemic levels during recirculation in contrast to normothermic cats. Hyperthermia without ischemia and hyperthermia during recirculation had no significant effect on intracellular pH. Thus, preischemic hyperthermia has a detrimental effect on metabolic recovery after transient global cerebral ischemia.

Topics: Acidosis; Adenosine Triphosphate; Animals; Brain Ischemia; Cats; Fever; Phosphates; Phosphocreatine

To assess the role of high-energy phosphate compounds in the etiology of heat injury with respect to the release of intracellular constituents, the susceptibility of selected tissues to heat injury, and the shock-like demise of the animals, rats were exercised on a treadmill (9.14 m/min) in a hot environment (34.5-35 degrees C) to a rectal temperature (Tre) of 42.5-43 degrees C. In the heart, kidney, left lateral lobe of the liver, and gastrocnemius muscle extricated from animals immediately upon termination of the treadmill run, levels of glucose-6-phosphate (G-6-P), adenosine triphosphate (ATP), and creatine phosphate (CP) were unchanged when compared with sedentary controls. In animals which had been resuscitated by infusion of isotonic saline into a jugular catheter, levels of CP were significantly (p less than 0.025) elevated in gastrocnemius muscle. In rats which were unconscious and succumbing to the effects of hyperthermic injury, levels of hepatic G-6-P and ATP were significantly reduced (p less than 0.05, p less than 0.02, respectively). These results indicate that the combination of exhaustive excercise/heat injury had the most deleterious effects upon hepatic metabolism. However, while resuscitation with physiological saline may be accompanied by an increased synthesis of CP, hyperthermic exhaustion and the concomitant efflux of cellular constituents cannot be attributed to a depletion or even a decrement of high-energy phosphates in vital tissues.

Topics: Adenosine Triphosphate; Animals; Fever; Glucosephosphates; Heat Exhaustion; Hindlimb; Hot Temperature; Kidney; Liver; Male; Muscles; Myocardium; Phosphocreatine; Physical Exertion; Rats; Sodium Chloride

Topics: Adenine Nucleotides; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Amino Acids; Animals; Body Water; Cerebral Cortex; Citric Acid Cycle; Fever; Glucose; Glycolysis; Hydrogen-Ion Concentration; Male; Oxygen Consumption; Phosphocreatine; Rats; Temperature

The influence of elevated and reduced body temperatures upon the metabolic state of the brain was evaluated from the tissue concentrations of phosphocreatine (PCr) ATP, ADP and AMP and from the concentrations of glucose, lactate and pyruvate in immobilized and artificially ventilated rats anesthetized with 70% N2O. The results were compared to the results obtained in normothermic animals. It was found that rats with body temperatures of 32 degrees and 22 degrees C had the same brain tissue concentrations of high energy phosphates and the same adenylate energy charge as the controls, but hypothermia led to a progressive decrease of both cerebral and arterial lactate and pyruvate concentrations. A metabolic acidosis but no excess lactate appeared in the blood. At a body temperature of 42 degrees C, the metabolic pattern in the brain agreed with a state of hypoxia at a time when there was no sign of substrate depletion. Arterial blood showed excess lactate which may indicate an inadequacy of the oxygen supply also to other tissues.

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Body Temperature; Brain; Carbon Dioxide; Energy Metabolism; Fever; Glucose; Hydrogen-Ion Concentration; Hypothermia; Lactates; Male; Oxygen; Oxygen Consumption; Partial Pressure; Phosphocreatine; Pyruvates; Rats

Topics: Adenine Nucleotides; Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Body Temperature; Brain Chemistry; Brain Stem; Catalepsy; Caudate Nucleus; Central Nervous System; Cerebral Cortex; Fever; Freezing; Humans; Male; Mice; Mice, Inbred Strains; Phosphocreatine; Reserpine; Spinal Cord; Temperature; Thalamus

Topics: Acid-Base Equilibrium; Adenosine Triphosphate; Animals; Body Temperature; Carbon Dioxide; Fever; Glucosephosphates; Hot Temperature; Hydrogen-Ion Concentration; Lactates; Muscles; Oxygen; Phosphocreatine; Physical Exertion; Rectum; Stress, Physiological; Swine; Swine Diseases