Biomedical subjects
Publications and source records attributed to K Wiśniewski.
A correlation between the postirradiation increase of the small intestine motility and the prostaglandin-like activity in this organ during gastrointestional syndrome was observed. Indomethacin decreased the elevated motility of intestine and reduced the prostaglandin-like activity in this syndrome.
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The influence of bradykinin and kallikrein on the action of norepinephrine, epinephrine, isoprenaline, phentolamine, propranolol, aminophylline and theophylline on blood pressure was studied. The kinins potentiated the hypertensive action of norepinephrine and epinephrine, weakened the hypotensive action of isoprenaline, potentiated the hypotensive action of propranolol, and had no effect on the action of phentolamine, aminophylline and theophylline.
Low molecular peptides, derived from fibrinogen digested by plasmin and injected either intraperitoneally or into the brain lateral ventricle, were found to act depressively on the CNS in active rats, while in fairly active rats they showed stimulatory effects. Fractionation of P-FDP on Sephadex G-25 showed that the most active peptides had a molecular weight lower than 5,000.
The effect of Fenchlorphos on postirradiation changes of serum protein levels and nucleic acid content in rat liver were investigated. It was found that this compound significantly decreases postirradiation changes in serum proteins, properdin level and nucleic acid content in rat liver. An important role of these phenomena in radioprotective action of Fenchlorphos is suggested.
The role of peptides such as fibrinogen degradation products (FDP), albumin degradation products (ADP), globulin degradation products (GDP), Bradykinin (BRS) and Angiotensin II (A) in CNS function is presented. Peptides change the activity of the CNS, of the centrally acting drugs and of some neuromediators. The mechanism of the phenomena observed is discussed.
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.
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The effect of fibrinopeptides A and B (FAB) on the action of compounds affecting the dopaminergic receptors in central nervous system (CNS) of rats was investigated. These peptides given intraperitoneally (ip) or intraventricularly (ivc) exerted dose-dependent stimulatory effects on the CNS: Enhanced the apomorphine and amphetamine-induced stereotypies and reduced the catalepsy induced by haloperidol. FAB depressed the dopamine level, especially when given together with alpha-MT, and elevated the level of homovanillic acid in the striatum. The results suggest that the stimulatory effects of FAB depend on their interaction with dopaminergic receptors in the CNS.
Indomethacin and fibrinogen degradation products (FDP) augmented amphetamine and apomorphine-induced stereotypies. In contrast, PGE1 and PGE2 decreased the stereotypies in rats, while PGF2 alpha enhanced amphetamine-induced stereotypy. Indomethacin given in combination with the peptides did not change their effect, whereas prostaglandins diminished the stimulatory effect of FDP on the amphetamine or apomorphine-induced stereotypy. Indomethacin and studied prostaglandins did not influence inhibitory action of FDP on haloperidol-induced catalepsy. It is concluded that prostaglandins do not play any essential role in the interaction of FDP with dopaminergic system in the CNS.
The activity of acetylcholinesterase was assessed in the rat brain in nephrogenic hypertension and after angiotensin administration. No significant differences were found in relation to corresponding control groups.
The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue). Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline. Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline. In animals receiving spiroperidol with bradykinin psychostimulatory action of noradrenaline was also not observed. FLA-63--inhibitor of dopamine beta-hydroxylase--increased the potentializing effect of bradykinin on the central action of dopamine. Most significant biochemical changes between the group receiving nialamide alone and the group given nialamide together with bradykinin have been observed in corpus striatum, where the level of dopamine and its metabolite--homovanillic acid--increased. The results obtained point out that the potentiation of the central effects of catecholamines by kinins depends mainly on the interaction of this peptide with dopaminergic receptor.
It has been found that kinins increase psychostimulatory effects of Nialamide and L-DOPA as well as psychoinhibitory effects of propranolol without any changes in phentolamine action. Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin.