Correlations between positive and negative aeroions, tissue redox-state potential and heart frequency in rats.

It was observed in rats that following positive aeroionization the redox-state potential (E'0) in skeletal muscles and liver was decreased, and the heart frequency increased. After negative ionization these interrelationships took place inversely. It was also established that upon adding an oxidant (menadione) i.v., the E'0 was decreased (compensatorily) in the organs mentioned above, parallel with the increment of heart frequency. Following injection of reductants (cysteine, thiamine) a reverse image was observed. Applying simultaneously positive ionization and reducing agents, the E'0 change and the heart frequency alteration failed to appear. The phenomenon was the same after simultaneous application of negative ionization and oxidant (menadione) injection. Because the heart effect of positive and negative ionization could readily be prevented by a respective redox agent, it seemed that actions of aeroions are exerted through shifts in tissue E'0. The most probable site of action of E'0, is the pacemaker mechanism, but an action on serotonin liberation may also be assumed.

Correlations between redox-state potential changes in different tissues and the heart frequency in vivo.

Redosis evoked in different tissues by methylene-blue or menadione (oxidants), resulted in an increase in heart frequency, while oxidosis evoked by thiamine or cysteine (reductants) diminished the frequency. In isolated organ tissues where compensatory redox feed back overshoots are rarely to develop, owing to the low redox buffer capacity and lack of the influence of nervous and humoral factors, the heart frequency decreased in response to direct oxidosis induced by the application of oxidants, and increased following reductant application; this suggested an environmental type redox regulatory influence of the agents rather than specific action of the agents. This environmental type effect can result from direct action on isolated organs, or from direct and indirect actions in vivo. An increased redox-state potential resulted in decreased heart frequency and inversely. In a pathological situation provoked by complete strangulation of aortae, a significant oxidosis developed in parallel with a decrease in heart frequency. On increasing the redox buffer capacity by application of methylene-blue (oxidant), or thiamine (reductant) both the redox and the resulting heart frequency changes could readily be counteracted. When cigarette smoke was pumped through an intratracheal tube, a significant redosis developed in the heart ventricle in parallel with an increased heart frequency. These data show that regardless of the origin of redox-state potential changes in tissues, a shift to oxidosis decreases and a shift to redosis increases the heart frequency.