[Experimental femur head necrosis of venous origin in the dog].
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Biomedical subjects
Publications and source records attributed to R Guiraud.
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Changes in the levels of amino acids in the plasma, liver and brain were studied in rats after simultaneous administration of 0.1 mmol/rat of arginine and aspartic acid. The levels of most of the assayed amino acids underwent various changes some of which only occurred in one of the organs studied, for example, GABA in the brain and proline in the liver. It is difficult to advance any explanation. Meanwhile some of changes can be explained on the grounds of well-known metabolic changes. The large increase of ornithine in the liver may be due to the action of arginase in the first stage in the urea cycle. This amino acid is the precursor of glutamic acid and proline which may explain the high levels of these two amino acids observed especially in the liver. The increase of GABA in the brain may be due to the simultaneous administration of arginine and aspartic acid which could induce the formation of ornithine and alpha-ketoglutaric acid respectively, two metabolites known to increase cerebral GABA. The increases in Ser, Gly, and Ala observed in practically all the tissues studied may be due to the formation of oxaloacetate from aspartic acid.
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The distribution of arginine and aspartic acid in brain, testes and liver was studied in rats after the simultaneous oral and intravenous administration of 0.1 mmol of these two amino acids. Exogenous fractions were determined by incorporation of [U-14C]-arginine and [3H]-aspartic acid. A significant increase in the free forms of the two amino acids was observed in all the organs except the liver where aspartic acid decreased after intravenous administration. The oral route induced higher concentrations of arginine in the testes and the brain and of aspartic acid in the liver. The concentrations of aspartic acid were higher in the brain and the testes after intravenous administration. Up to 15% of the dose of arginine administered was found in the liver, most of it bound to protein. Free aspartic acid concentrations underwent two successive increases with return to baseline values between the two phases. The first phase seemed to be due to an accumulation of the amino acid in the organ, followed by binding of the amino acid to the proteins. The second increase seemed to be due to a displacement of the protein bound form towards the free form. The steep rise in cerebral arginine levels, peaking at 30 minutes, may be one of the determining factors governing GH secretion induced by the simultaneous oral administration of aspartic acid and arginine.
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