The effect of hyperbaric oxygen on the GABA shunt pathway in brain homogenates

1968 ◽  
Vol 46 (4) ◽  
pp. 669-671 ◽  
Author(s):  
W. S. Myles ◽  
J. D. Wood
Keyword(s):  
High Pressure ◽  
Rat Brain ◽  
Ambient Pressure ◽  
Aminobutyric Acid ◽  
Gaba Shunt ◽  
In Vitro Method ◽  
Shunt Pathway ◽  
Effect Of Oxygen ◽  
Small Inhibition

The effect of oxygen at high pressure (OHP) on the γ-aminobutyric acid (GABA) shunt pathway in rat brain homogenates was studied by measuring the formation of labelled succinate from GABA-4-14C in the presence of malonate. Under in vitro conditions, OHP inhibited the GABA shunt by 28% and 22%, with and without the addition of supplementary amounts of GABA and α-ketoglutarate to the incubation media respectively. A small inhibition (10%) was also observed with oxygen at ambient pressure. In further studies, rats were exposed to OHP, and the activity of the GABA shunt in the brains was subsequently measured by the in vitro method. Preexposure of the intact animals, with or without accompanying convulsions, did not affect the metabolism of GABA to succinate.

Oxidative metabolism of incubated cerebral cortex slices from pyridoxine-deficient kittens

1961 ◽  
Vol 200 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Guy M. McKhann ◽  
Olaf Mickelsen ◽  
Donald B. Tower
Keyword(s):  
Cerebral Cortex ◽  
Oxygen Uptake ◽  
Oxidative Metabolism ◽  
Pyridoxal Phosphate ◽  
In Vitro Study ◽  
Aminobutyric Acid ◽  
Shunt Pathway ◽  
Pyridoxine Deficiency ◽  
Cortex Slices

Pyridoxine deficiency was produced in weanling kittens by dietary means. Clinically, the deficient animals showed failure to gain weight, ataxia, and, if left on the diet, seizures and death. In vitro study of isolated cerebral cortex slices from the deficient animals showed decreased formation of γ-aminobutyric acid and decreased oxygen uptake when glucose was the substrate. Addition of pyridoxal phosphate to the incubation media corrected both of these defects toward the levels found in normal littermate controls. The decreased oxygen uptake was also corrected by the addition of γ-aminobutyric acid to the media. It is suggested that in pyridoxine deficiency, cerebral oxidative metabolism is impaired by blockage of the γ-aminobutyric acid ‘shunt’ pathway at the glutamic decarboxylase step. The role of this shunt pathway in normal neuronal metabolism is discussed.

Convulsions and the γ-aminobutyric acid content of rat brain

1968 ◽  
Vol 46 (5) ◽  
pp. 803-804 ◽  
Author(s):  
F. V. DeFeudis ◽  
K. A. C. Elliott
Keyword(s):  
High Pressure ◽  
Rat Brain ◽  
Acid Content ◽  
Aminobutyric Acid ◽  
The Brain

The observation of Wood and Watson that the γ-aminobutyric acid content of the brain decreases in animals that suffer convulsions during treatment with oxygen at high pressure has been confirmed. This decrease is prevented when seizures are prevented by prior intraperitoneal injections of hyperosmotic solutions. When seizures are induced by picrotoxin or pentylenetetrazol the GABA levels are slightly (and alanine levels considerably) increased.

GAMMA-AMINOBUTYRIC ACID LEVELS IN THE BRAIN OF RATS EXPOSED TO OXYGEN AT HIGH PRESSURES

1963 ◽  
Vol 41 (9) ◽  
pp. 1907-1913 ◽  
Author(s):  
J. D. Wood ◽  
W. J. Watson
Keyword(s):  
High Pressure ◽  
Recovery Time ◽  
High Pressures ◽  
No Reduction ◽  
Ambient Pressure ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Concentration ◽  
Short Period ◽  
The Brain

Rats were exposed to 100% oxygen at a pressure of 6 atmospheres absolute for 33 minutes. The surviving animals were assigned to one of three groups: (a) animals suffering severe convulsions during exposure, (b) animals suffering mild convulsions during exposure, (c) animals in which no convulsions were observed during exposure. The concentration of gamma-aminobutyric acid (GABA) in the brains of rats in all groups was lower than in unexposed rats, reductions of 35%, 27%, and 19% in GABA concentration being observed in groups (a), (b), and (c) respectively. Only a few minutes' exposure to oxygen at high pressure was necessary to cause a significant decrease in GABA concentration. Exposure either to air at high pressure or to 100% oxygen at ambient pressure produced no reduction in GABA levels. Although the GABA concentration in the brain increased markedly within 1 hour after the end of the 33-minute exposure to oxygen at 6 atm pressure it was still somewhat below the levels found in unexposed animals. No significant change in GABA levels was observed during a further 2 hours of recovery time. In the case of rats exposed for only a short period of time, however, a complete return to normal was observed within the first hour. The levels of glutamic acid, aspartic acid, and total α-amino acids in the brain were not altered by exposure to oxygen at high pressure.

GAMMA-AMINOBUTYRIC ACID LEVELS IN THE BRAIN OF RATS EXPOSED TO OXYGEN AT HIGH PRESSURES

1963 ◽  
Vol 41 (1) ◽  
pp. 1907-1913 ◽  
Author(s):  
J. D. Wood ◽  
W. J. Watson
Keyword(s):  
High Pressure ◽  
Recovery Time ◽  
High Pressures ◽  
No Reduction ◽  
Ambient Pressure ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Concentration ◽  
Short Period ◽  
The Brain

Rats were exposed to 100% oxygen at a pressure of 6 atmospheres absolute for 33 minutes. The surviving animals were assigned to one of three groups: (a) animals suffering severe convulsions during exposure, (b) animals suffering mild convulsions during exposure, (c) animals in which no convulsions were observed during exposure. The concentration of gamma-aminobutyric acid (GABA) in the brains of rats in all groups was lower than in unexposed rats, reductions of 35%, 27%, and 19% in GABA concentration being observed in groups (a), (b), and (c) respectively. Only a few minutes' exposure to oxygen at high pressure was necessary to cause a significant decrease in GABA concentration. Exposure either to air at high pressure or to 100% oxygen at ambient pressure produced no reduction in GABA levels. Although the GABA concentration in the brain increased markedly within 1 hour after the end of the 33-minute exposure to oxygen at 6 atm pressure it was still somewhat below the levels found in unexposed animals. No significant change in GABA levels was observed during a further 2 hours of recovery time. In the case of rats exposed for only a short period of time, however, a complete return to normal was observed within the first hour. The levels of glutamic acid, aspartic acid, and total α-amino acids in the brain were not altered by exposure to oxygen at high pressure.

A in Vivo Assay for Standardizing Heparin Preparations

1979 ◽  
Vol 41 (03) ◽  
pp. 576-582
Author(s):  
A R Pomeroy
Keyword(s):  
In Vitro Assays ◽  
British Pharmacopoeia ◽  
In Vitro Method ◽  
Standard Preparation ◽  
Reliable Estimation ◽  
Assay Procedure ◽  
Accuracy And Precision ◽  
Heparin Preparation

SummaryThe limitations of currently used in vitro assays of heparin have demonstrated the need for an in vivo method suitable for routine use.The in vivo method which is described in this paper uses, for each heparin preparation, four groups of five mice which are injected intravenously with heparin according to a “2 and 2 dose assay” procedure. The method is relatively rapid, requiring 3 to 4 hours to test five heparin preparations against a standard preparation of heparin. Levels of accuracy and precision acceptable for the requirements of the British Pharmacopoeia are obtained by combining the results of 3 to 4 assays of a heparin preparation.The similarity of results obtained the in vivo method and the in vitro method of the British Pharmacopoeia for heparin preparations of lung and mucosal origin validates this in vivo method and, conversely, demonstrates that the in vitro method of the British Pharmacopoeia gives a reliable estimation of the in vivo activity of heparin.

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