Effects of pyrasidol (1,10-trimethylen-8-methyl-1,2,3,4-tetrahydropyrasino(1,2-a) indol hydrochloride)--a selective reversible inhibitor of monoaminoxidase (MAO)--on substrate specificity of MAO fragments of mitochondrial membranes of the rat liver in altitude chamber hypoxia were studied. It is shown that pyrasidol during hypoxic exposure causes a sharp initial decrease of functional activity of type A MAO in the rat liver and its subsequent significant increase, i.e., elevates reserve potentialities of monoaminergic neuromediation which, along with a selective inhibition of oxidation of biogenic amines and activation oxidative deamination of other nitrogenous compounds, contributes to better survival rate in animals in hypoxic environment.
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