Correlations between the actual redox-state potential (E0') of biophase and heart activity in vivo.
In CFY rats the tissue redox-state potential (E0') in heart, m. vastus medialis and in the liver, and the heart frequency and QRS amplitudes were measured parallel. It was observed that following compensatory redosis caused by konakion both the autorhythmic heart frequency and QRS amplitudes increased, while after compensatory oxidosis induced by urea occurred the opposite. Following compensatory redosis caused by konakion acetylcholine decreased, but adrenaline increased the heart frequency and QRS amplitudes more intensively than at normal E0' values. After compensatory oxidosis caused by urea, acetylcholine decreased the heart frequency and QRS amplitudes significantly less. Adrenaline decreased the heart frequency in such milieu. On the basis of these data the following conclusions are proposed; For the realization of autorhythmic activity, for negative type acetylcholine and for positive type adrenaline effects in heart, a relatively low primordial tissue E0' value is an essential back-ground element. Among the mechanisms controlling autorhythmicity and sympathetic/parasympathetic effects the actual and permanently changing tissue E0' value is also an important modifying, or through biochemical redox feed-back mechanisms even a regulatory factor of heart activity.
Puppi
A
A
Central Laboratory of Animal Research, University Medical School, Hungary.
Dely
M
M
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004562:Electrocardiography / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D008099:Liver / Q000502:physiology; D010084:Oxidation-Reduction; D051381:Rats; D010837:Vitamin K 1 / Q000494:pharmacology
D010837:Vitamin K 1; D000109:Acetylcholine; D004837:Epinephrine