phosphocreatine and Carbon-Monoxide-Poisoning

We studied muscle blood flow, muscle oxygen uptake (VO(2)), net muscle CO uptake, Mb saturation, and intracellular bioenergetics during incremental single leg knee-extensor exercise in five healthy young subjects in conditions of normoxia, hypoxia (H; 11% O(2)), normoxia + CO (CO(norm)), and 100% O(2) + CO (CO(hyper)). Maximum work rates and maximal oxygen uptake (VO(2 max)) were equally reduced by approximately 14% in H, CO(norm), and CO(hyper). The reduction in arterial oxygen content (Ca(O(2))) (approximately 20%) resulted in an elevated blood flow (Q) in the CO and H trials. Net muscle CO uptake was attenuated in the CO trials. Suprasystolic cuff measurements of the deoxy-Mb signal were not different in terms of the rate of signal rise or maximum signal attained with and without CO. At maximal exercise, calculated mean capillary PO(2) was most reduced in H and resulted in the lowest Mb-associated PO(2). Reductions in ATP, PCr, and pH during H, CO(norm), and CO(hyper) occurred earlier during progressive exercise than in normoxia. Thus the effects of reduced Ca(O(2)) due to mild CO poisoning are similar to H.

Topics: Adenosine Triphosphate; Adult; Arteries; Capillaries; Carbon Monoxide Poisoning; Carboxyhemoglobin; Energy Metabolism; Exercise; Humans; Hydrogen-Ion Concentration; Magnetic Resonance Imaging; Male; Muscle, Skeletal; Myoglobin; Oxygen Consumption; Phosphocreatine; Regional Blood Flow; Veins

Parkinsonism is a common neurological sequela of carbon monoxide (CO) poisoning, but its pathophysiological mechanism has yet to be clarified.. To describe a married couple who were both affected by CO poisoning, but only 1 of whom developed CO-induced parkinsonism, and to discuss the possible underlying pathophysiological mechanism of CO-induced parkinsonism by comparing the neuroimaging findings of these patients.. Case report from a clinical neurology department.. A married couple experienced CO poisoning simultaneously. One month later, only the husband gradually developed delayed sequelae, including parkinsonism and intellectual impairment. On detailed neurological examination, the husband showed mild but definite rigidity and bradykinesia, while no parkinsonian signs were observed in the wife. Neuropsychological examination revealed impaired memory and attention in both patients, but they were more severe in the husband than in the wife. Magnetic resonance imaging scans of the patients' brains disclosed diffuse high-intensity white matter signals in both patients and bilateral pallidal necrosis in the wife. Dopamine transporter imaging showed that the degree of dopamine neuronal loss was comparable between these patients. Magnetic resonance spectroscopy revealed more severe white matter damage in the husband than in the wife. Thirteen months later, neurological and neuropsychological examinations showed complete recovery from parkinsonism as well as intellectual impairment. Follow-up magnetic resonance spectroscopy also suggested remarkable improvements in white matter damage.. These results support the role of white matter damage in producing parkinsonism after CO poisoning and highlight the possible usefulness of magnetic resonance spectroscopy in predicting delayed sequelae in patients after CO poisoning. Arch Neurol. 2000;57:1214-1218

Topics: Aspartic Acid; Brain Chemistry; Carbon Monoxide Poisoning; Carrier Proteins; Choline; Cognition Disorders; Dopamine Plasma Membrane Transport Proteins; Female; Humans; Magnetic Resonance Imaging; Male; Membrane Glycoproteins; Membrane Transport Proteins; Middle Aged; Nerve Tissue Proteins; Parkinson Disease; Phosphocreatine; Tomography, Emission-Computed, Single-Photon

Brain energy metabolites were determined in mice over 8 days after an acute exposure to carbon monoxide (CO). The exposure of 0.5% CO for 15 min caused 33% mortality. Survived mice recovered completely within 30 min in room air. Lactate increased markedly immediately after the exposure, while glucose increased 30 min later. Four hours, 1 day, 4 days and 8 days after the exposure, the levels of brain energy metabolites including phosphocreatine and ATP did not differ from those of the control. Thus, energy metabolism in the whole brain in mice appears not to be impaired after they survive an acute CO intoxication.

Topics: Adenosine Triphosphate; Animals; Brain; Carbon Monoxide Poisoning; Carboxyhemoglobin; Energy Metabolism; Glucose; Lactates; Lactic Acid; Male; Mice; Phosphocreatine

The effects of 1 h exposure to 1% CO and right common carotid artery clamping upon the cerebral energy metabolism, perfusion and histology were studied in anesthetized (70%N(2)O) and unanesthetized rats following reoxygenation for 0-6 h. At 0 h recovery the clamped hemispheres showed decreases of ATP, PCr and glycogen, and increases of ADP, AMP, inorganic phosphate and lactate which indicated an advanced derangement of the tissues' energy homeostasis. Exposure in unanesthetized animals was associated with lower levels of ATP and glycogen, and with larger increases of lactate in the clamped hemisphere which suggested the presence of a more intense hypoxic-oligemic insult. The metabolic differences in the clamped hemisphere of unanesthetized and anesthetized animals became more marked after 1 h reoxygenation, with anesthetized animals showing large restitutions of ATP, PCr, glycogen and lactate, whereas in unanesthetized animals these metabolites showed severe persistent defects over the 6 h reoxygenation period. Since the arterial oxygen content and tension, and perfusion patterns were equivalent in the 2 series at 0 and 1 h recovery, it is concluded that even minor anesthetic agents such as 70%N(2)O or other non-hypoxic variables during exposure or recovery may cause significant alterations in the metabolic restitution of the hypoxic-oligemic brain.

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Brain; Carbon Dioxide; Carbon Monoxide; Carbon Monoxide Poisoning; Carotid Arteries; Cerebrovascular Circulation; Energy Metabolism; Glycogen; Hypoxia, Brain; Male; Oxygen; Phosphates; Phosphocreatine; Rats

Topics: Adenosine Triphosphate; Animals; Blood Pressure; Brain; Carbon Monoxide; Carbon Monoxide Poisoning; Carboxyhemoglobin; Colorimetry; Energy Metabolism; Environmental Exposure; Lactates; Liver; Male; Oxygen; Partial Pressure; Phosphocreatine; Pyruvates; Rats

Topics: Acute Disease; Adenosine Triphosphate; Animals; Blood Glucose; Brain; Carbohydrate Metabolism; Carbon Monoxide Poisoning; Chronic Disease; Female; Glycogen; Lactates; Phosphocreatine; Pyruvates; Rats

Topics: Acidosis; Adenosine Triphosphate; Alkalosis; Animals; Brain; Carbon Monoxide Poisoning; Glycolysis; Hemoglobins; Lactates; Mice; Phosphocreatine; Pyruvates; Sodium; Succinates