ABSTRACT
The sympatho-adrenergic reaction was investigated in heated rats under the influence of a ganglioblocking agent--hexamethonium. The overheating at a 40 degrees environmental temperature produced in a relatively short interval (after 157 min on an average) the death of the animals. An initial bradycardia was followed by a tachycardic phase. In the prelethal phase there appeared bradyarrhythmia produced by conductibility troubles and activation of ectopic ventricular centers. The survival time was not influenced by hexamethonium in spite of its hypothermic action. In blood, heating produced an increased concentration of noradrenaline and adrenaline. Hexamethonium, which reduced the rectal temperature, markedly decreased both blood catecholamines concentration. On this background heating likewise produced a relative increase of both blood catecholamines content. The catecholamines changes in adrenal glands presented less significant modifications.
Subject(s)
Arrhythmias, Cardiac/etiology , Fever/physiopathology , Heart Conduction System/physiopathology , Hexamethonium Compounds/pharmacology , Sympathetic Nervous System/physiopathology , Animals , Catecholamines/blood , Electrocardiography , Fever/complications , Heart/physiopathology , RatsABSTRACT
Rats exposed for different intervals (1, 3 and 6 hours, the first day, and then 6 hours a day for 9 days) to a 2200-m hypoxia presented metabolic changes demonstrating an anaerobic glucose utilization. Thus, in accordance with other authors, at different depressurization values the liver homogenate had increased lactate and pyruvate concentrations, decreased NAD and NADH2 concentrations and a decreased ATP formation, demonstrating the inefficient glucide metabolization. These modifications were evident in the first hours of depressurization, but did not occur under acclimatization during the 9 days of exposure. The LDH concentration remained practically unchanged, which might be explained by its explained by its excessive presence in relation to the normal exercise solicitation. A urinary hypercompensatory alkalinization was also recorded.
Subject(s)
Altitude , Carbohydrate Metabolism , Hypoxia/metabolism , Adenosine Triphosphate/metabolism , Animals , Glucose/metabolism , L-Lactate Dehydrogenase/metabolism , Lactates/metabolism , Liver/metabolism , Liver Glycogen/metabolism , NAD/metabolism , Pyruvates/metabolism , RatsSubject(s)
Circadian Rhythm , Liver/enzymology , Radiation Effects , Tyrosine Transaminase/radiation effects , Animals , Enzyme Induction , Male , MiceABSTRACT
On X-ray irradiated mice with a total dose of 800 R, the reactivity upon an aggressive agent (chloroform stress) administered at various delays after irradiation was studied. The reactivity of the animals has been emphasized by the hepatic induction of the tyrosine aminotransferase and by the adrenal ascorbic acid depletion. From the 3rd day after irradiation both these parameters showed a marked and irreversible decrease.
Subject(s)
Liver/enzymology , Radiation Injuries, Experimental/enzymology , Stress, Physiological/enzymology , Tyrosine Transaminase/metabolism , Animals , Chloroform , Enzyme Induction , Liver/radiation effects , Mice , Stress, Physiological/chemically inducedSubject(s)
Infant, Newborn, Diseases , Metabolism, Inborn Errors , Amines/metabolism , Amino Acid Metabolism, Inborn Errors , Ascorbic Acid/metabolism , Carbohydrate Metabolism, Inborn Errors , Female , Glucose/metabolism , Humans , Infant , Infant, Newborn , Lipid Metabolism, Inborn Errors , Male , Peptides/metabolism , Phosphatidylcholines/metabolism , Ribose/metabolismABSTRACT
In experiments carried out in male Wistar rats submitted in laboratory to a 2200-m depressurization the urinary noradrenaline and adrenaline elimination, as well as the plasma corticosterone level were investigated. In rats previously submitted 12 days only to the environmental stress the true depressurization (7 days) produced a relatively increased noradrenaline and adrenaline elimination. A similar increased catecholamine output was observed in rats submitted directly to hypoxia. The plasma corticosterone level was unmodified by hypoxia of the same value.
