[Mefacit-induced pancytopenia].
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Biomedical subjects
Publications and source records attributed to A Bodzenta.
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The influence of PGE1 and its precursor dihomo-gamma-linolenic acid on the central action of acetylcholine was studied. PGE, and dikomo-gamma-linolenic acid increased the depressive action of acetylcholine as evaluated with Lat's and thiopental sleeping time tests. PGE1 and its precursor diminished or eliminated the influence of acetylcholine on pentetrazol convulsions. Endogenous acetylcholine in excess inhibited hyperthermic effect of PGE1. The results show that PGE1 and its precursor may change the action of acetylcholine in the central nervous system.
The interaction between kinins formed in central nervous system and acetylcholine was studied. Endogenous ACh in excess acted psychodepressively on the animal's behavior as evaluated with Lat's test. This effect was more intense in those rats in which the activity of kinin-forming enzymes in the nervous tissue had been increased with either kallikrein or bradykinin. Both kallikrein and bradykinin intensified the psychodepressive action of exogenous ACh given into the brain ventricle. Results show that kinins can enhance the inhibitory central action of ACh.
Kallikrein given in combination with acetylcholine (ACh) increased the central inhibitory action of ACh as measured in the Lat's test, duration of thiopental sleep and inhibition of electrogenic convulsions. Indomethacin aboished the potentiating effect of kallikrein on these actions of ACh, PGE1 did not play a significant role in the influence of kallikrein on the central action of ACh. However, inhibition of prostaglandin synthesis with indomethacin plays an important role in the interaction of kallilkrein and ACh.