Effect of adrenalectomy on convulsions induced by high-pressure oxygen

1979 ◽  
Vol 57 (7) ◽  
pp. 688-694 ◽  
Author(s):  
A. K. Singh ◽  
E. W. Banister

Adrenalectomized rats exposed to high pressure oxygen (OHP) until convulsion convulse much later than sham-operated or normal rats. No significant changes in the concentration of noradrenaline (NA) and total catecholamines (TC) in the brain were noted in sham-operated or adrenalectomized rats resulting from sham or real surgery and no change occurred in these variables in normal sham-operated or adrenalectomized animals after OHP leading to convulsion. Brain adrenaline (A) concentration, however, decreased significantly in all three groups following OHP-induced convulsions. Activity of catecholamine O-methyltransferase (COMT) decreased significantly only in adrenalectomized rats. Brain γ-aminobutyric acid (GABA), glutamate, and other amino acid level remained unchanged after adrenalectomy whereas the concentration of ammonia decreased significantly when normal rats were adrenalectomized. After OHP-induced convulsions, the concentrations of brain GABA and glutamate decreased and ammonia and glutamine plus asparagine increased significantly in normal, sham-operated, and adrenalectomized rats. In the blood no significant difference was noted in the concentration of the catecholamines, ammonia, and amino acids either in normal or sham-operated rats. In adrenalectomized rats, the blood A and NA concentrations decreased significantly and tyrosine increased significantly. The concentration of NA, ammonia, and glutamine plus asparagine in rats from all three groups increased after OHP-induced convulsions, whereas the concentration of glutamate decreased significantly. Since the concentration of A increased significantly after convulsions in normal and sham-operated rats but did not change in adrenalectomized rats, it might be proposed that adrenalectomy protects against OHP-induced convulsions by reducing the circulating concentration of A and ammonia.However, these are not the only factors involved in the protection since the sham-operated rats also convulsed much later than normal rats but had similar ammonia and A concentrations to normal animals.

1979 ◽  
Vol 57 (4) ◽  
pp. 390-395 ◽  
Author(s):  
E. W. Banister ◽  
A. K. Singh

The time course of changes in blood and brain catecholamines, catechol (O-methyltransferase (COMT), ammonia, and amino acids leading to convulsion by high pressure oxygen breathing (OHP) in rats has been investigated. Brain catecholamines were suppressed by OHP. They changed in phase with brain COMT concentration and consequently were not due to the action of this degrading enzyme. Convulsive actions seem not to be influenced by brain catecholamine concentration. Blood adrenaline concentrations are, however, significantly elevated both prior to and during convulsions. In both brain and blood, ammonia concentration increases, glutamate decreases, and glutamine–aspargine increases. It is proposed that the efficacy of the glutamate–glutamine ammonia buffering system in blood and brain is important in the prevention of the onset of convulsions but that when brain γ-aminobutyric acid is depressed to critical levels, convulsions result.


1978 ◽  
Vol 56 (2) ◽  
pp. 334-336 ◽  
Author(s):  
A. K. Singh ◽  
E. W. Banister

Effects of 6-hydroxydopamine (6-OHDA) on rat brain and blood adrenaline (A), noradrenaline (NA), ammonia (NH3), γ-aminobutyric acid (GABA), and amino acid metabolism prior to and after high pressure oxygen (OHP) induced convulsions have been studied. 6-OHDA reduces GABA and glutamate (Glu) prior to OHP exposure in rat brain so that the concentration is even equal to that seen in nondrugged animals after convulsion. Concomitantly, 6-OHDA reduces the latency of OHP-induced convulsion significantly, and increases brain NH3, glutamine, and asparagine significantly. Although 6-OHDA, in increasing dosage, elevates blood A concentration, convulsion produces a significant further increase in A. Blood NA was not significantly changed in drugged, convulsed animals and was much less than blood NA concentrations in nondrugged convulsed animals. Increasing doses of 6-OHDA also increase NH3 in the blood significantly and convulsion increases its concentration further. Latency of convulsion seems to be related to certain monoamine levels since in some drugged animals where A and total catecholamines are still reduced 96 h after the first of two doses of 6-OHDA, NA concentrations are recovered to relatively normal and the convulsion latency time is also increased although it remains significantly abbreviated from undrugged animals' convulsion time. Low brain GABA levels seem to be a prime effector of convulsive activity.


Author(s):  
Brian Drouin ◽  
Jiajun Hoo ◽  
V. Devi ◽  
D. Benner ◽  
David Robichaud ◽  
...  

2001 ◽  
Author(s):  
B. Vyskubenko ◽  
A. Adamenkov ◽  
S. Ilyin ◽  
Yu. Kolobyanin ◽  
I. Krukovsky ◽  
...  

2010 ◽  
Vol 447-448 ◽  
pp. 61-65 ◽  
Author(s):  
Kei Kitamura ◽  
Toshiro K. Doi ◽  
Syuhei Kurokawa ◽  
Yoji Umezaki ◽  
Yoji Matsukawa ◽  
...  

We designed and manufactured a prototype of a unique CMP machine, which can perform double-side CMP simultaneously in a sealed and pressure container as regarding effective action of the processing atmosphere around workpieces as important. Polishing experiments with single crystal silicon (Si) wafers (100) are performed by charging the container with various gases. As a result, the removal rates increased by up to 25% under high pressure oxygen gas atmosphere.


1992 ◽  
Vol 89 (2) ◽  
pp. 221-228 ◽  
Author(s):  
Theodore A. Steinberg ◽  
George P. Mulholland ◽  
D.Bruce Wilson ◽  
Frank J. Benz

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