Changes in balance of biogenic monoamines and their metabolites in rats with hyperbaric epilepsy

Abstract

A protective role of monoamine oxidase inhibitors in hyperbaric epilepsy has been reported [2], confirming involvement of the brain monoaminergic systems in the development of seizure activity. However, changes in the balance of monoamines and their metabolites in different phases of the epileptiform seizure have not yet been studied~ Moreover, there are virtually no data on the role of monoaminergic systems of the heart in the genesis of oxygen poisoning. The aim of this investigation was to study changes in concentrations of biogenic amines and their metabolites in certain parts of the brain and heart of rats exposed to a session of toxic hyperbaric oxygenation of varied duration. EXPERIMENTAL METHOD Biogenic amines and their metabolites were determined by high-performance liquid chromatography (HPLC) with electrochemical detection [4]. The convulsive form of oxygen poisoning was induced by exposing noninbred male albino rats in a pressure chamber to oxygen in a pressure of 6 atm for 5-60 min. Periods of compression and decompression each lasted 20 min. At the end of decompression the rats were decapitated and brain and heart structures were removed in the cold and kept in liquid nitrogen until use. EXPERIMENTAL RESULTS Three stages of hyperbaric epileptic fit were investigated: compensatory (exposure for 5 min), convulsive (exposure 27 min), and terminal (exposure 60 min). The results are given in Tables I and 2. It will be Clear from Tables 1 and 2 that under normal circumstances the concentration of catecholamine (CA) metabolites in the rat heart was much lower than in the brain: in the left and right ventricles homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DHPAA) were absent; no 3-methoxy-4-hydroxyphenylglycol (MHPEG) could be found and the 5-hydroxyindoleacetic acid (5-HIAA) level was very low. Compared with the left ventricle, the right contained more 3,4-dihydroxyphenylglycol (DHPEG), noradrenalin (NA), and adrenalin (A), but less dihydroxyphenylalanine (DOPA). No metabolites of dopamine (DA) were present in the ventricles of the heart, but its precursor (DOPA) was present. No 3,4-dihydroxymandelic acid (DHMA) was found in the atria (total preparation), but concentrations of serotonin (5-HT) and 5-HIAAwere significantly higher than in the ventricles; metabolites of DA, and also MHPEG, were absent but the DOPA concentration was lower than in the left ventricle but higher than in the right. In the septum of the heart concentrations of NA and A were much lower than in the ventricles and atria; neither DHMA nor HVA was found, but DHPAA was present in higher concentrations that in other parts of the heart, but the 5-HIAA concentration was very low. The results showing the distribution of monoamines and their metabolites in the normal rat brain and heart justify the conclusion that the principal monoaminergic substances in the rat heart are NA and A, and that virtually all the monoamines and their metabolites studied are well represented in the brain.