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Biomedical subjects

C Maśliński

Publications and source records attributed to C Maśliński.

At least 19 recordsLinked to original sources
PubMed1978

An interaction of histamine H2-receptor antagonists with the noradrenergic system in rat brain.

Intraventricular administration of 50 microgram of burimamide or 250 microgram of either metiamide or cimetidine decreased the NA concentration in rat hypothalamus by nearly 30%. Cimetidine did not significantly influence either DA or DOPAC levels in striatum. Cimetidine and metiamide significantly potentiated locomotor activity of tranylcypromine-treated rats and this effect was antagonized by phentolamine. It is concluded that the three histamine H2-receptor antagonists released NA in rat brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Conditions for the formation of cyclic compounds between pyridoxal phosphate and 5-hydroxytryptamine or 5-hydroxytryptophan.

5-Hydroxytryptamine (5HT) and 5-hydroxytryptophan (5HTP) form cyclic compounds (probably of the tetrahydro-beta-carboline type) with pyridoxal phosphate (PLP). In the first step of reaction a Schiff's base is formed; during incubation it is transformed into a cyclic compound with a maximum absorption spectrum at 330 nm. The degree of cyclization depends on pH and substrate concentrations. One mole of 5HT or 5HTP reacts with one mole of coenzyme. The velocity of cyclization increased with an excess of either 5HT (5HTP) or PLP, without any change in the mole to mole ratio. The formation of cyclic compounds was confirmed by the use of isotopes, separation from substrates being achieved by high-voltage electrophoresis.

5-Hydroxytryptophan↗
PubMed1978

Phosphopyridoxal cyclic compounds with histamine and histidine. 6: The formation of phosphopyridoxal cyclic compounds with histamine and histidine in the presence of biological material.

We have studied the dynamics of cyclic compound formation between histamine or histidine and pyridoxal 5'-phosphate (Hi-PLP or His-PLP) in incubates of rat gastric mucosa histidine decarboxylase (HD), rat intestinal diamine oxidase (DAO) or homogenates of either rat liver, intestine or gastric mucosa. For gastric mucosa HD, liver and gastric mucosa homogenates, the rate of cyclization was slightly decreased; however, the rate was significantly inhibited with intestinal DAO or intestinal homogenate. Binding of PLP by tissue components was measured; free PLP was bound abundantly by rat intestinal DAO and by rat intestinal homogenate. A possible mechanism by which intestinal tissues inhibit cyclic compound formation is discussed.

Amine Oxidase (Copper-Containing)↗
PubMed1978

Phosphopyridoxal cyclic compounds with histamine and histidine. 7: The properties of pyridoxal and phosphopyridoxal cyclic compounds with histamine and histidine.

Cyclic compounds synthesized from histamine (Hi) or histidine (His) with pyridoxal (PL)--[Hi-PL, His-PL] and Hi or His with pyridoxal 5'-phosphate (PLP)--[Hi-PLP, His-PLP] were tested for stability in buffer, acid and base solutions, crude homogenates of various tissues and in the presence of enzymes which metabolize Hi or His. The cyclic pyridoxal compounds were stable in all experimental conditions, whereas phosphopyridoxal cyclic products were degraded by rat intestinal DAO and rat intestine homogenate, apparently enzymatically. In acidic and basic solutions changes in migration velocity and u.v. absorption spectrum occur. The characteristic fluorescence of these cyclic compounds is described.

Animals↗
PubMed1978

Reaginic sensitization of mice and rats.

The reagin response to hemocyanin (KLH) and egg albumin (EA) was studied in inbred strains (Balb/c, 129, C3H/A, C57BL/6J) and Swiss-Copacabana mice. Both antigens induced apparent and in certain experimental conditions, persistent reagin production, KLH being more effective. Al(OH)3 gel as an adjuvant was more suitable for IgE antibody production, while the Freund's complete adjuvant appeared more appropriate for IgG1 antibody response. The reaginic response to EA and Al(OH)3 in rats Wistar, Sprague-Dawley and F1 hybrids (Wistar x August) was weak and transient. The best sensitization, though relatively low as compared with mouse sensitization, was obtained in Sprague-Dawley and F1 hybrids. The results suggest, that a mouse model of sensitization is quite suitable for studying the persistent reagin response, while a rat model may be useful for investigating the early suppression of reagin response.

Adjuvants, Immunologic↗
PubMed1978

Passive sensitization of mice and rats with IgE antibodies.

The strain-dependent variation in susceptibility to passive sensitization of the skin and peritoneal mast cells with homologous IgE antibodies was observed in inbred strains of mice. Strain 129 showed low susceptibility to passive sensitization and high efficiency of normal serum in blocking mouse reagin-induced PCA in rats. Balb/c and C3H/A strains showed higher susceptibility to passive sensitization and the efficiency of normal serum in blocking rat PCA lower than strain 129. The serum factor responsible for rat PCA inhibiting effect was heat-labile. The anaphylactic response of peritoneal mast cells of inbred strains to the challenge with anti-mouse IgE and anti-rat IgE in vitro was low in Balb/c mice, as compared with the response of C57BL/6J and 129 mice. The results suggest, that non-specific IgE present in the serum or bound to the mast cells may be one of the factors determining the susceptibility of mouse strains to reagin-induced passive sensitization. However, the results obtained with C57BL/6J strain suggest the existence of other factors effecting this susceptibility.

Animals↗
PubMed1978

Effect of complexes of lidocaine with transient metals on histamine release from rat mast cells.

The effect of complexes of lidocaine with zinc, copper and cobalt on histamine release from peritoneal rat mast cells induced by various secretagogues was investigated. The complexes of lidocaine with metal ions inhibited histamine release induced by compound 48/80 and ionophoreous antibiotics: A23187 and X537A. The ionic complex of lidocaine with zinc was found to be the most potent against 48/80--induced histamine release and exerted the significant inhibition in the concentration of 10(-5) M. The action of coordination complex of lidocaine with zinc was somewhat weaker. The significant inhibitory effect on 48/80-induced histamine release of the copper and cobalt lidocaine complexes was observed in concentration of 10(-4) M. Histamine release by ionophores A23187 and X537A was also affected by zinc lidocaine complexes. However, coordination complex had more potent action on histamine release than the ionic one.

Animals↗
PubMed1977

Phosphopyridoxal complexes with histamine and histidine. (5) The kinetics of cyclic compound formation between histamine and pyridoxal-5'-phosphate in the presence of pig kidney diamine oxidase and rat intestinal histaminase.

Pig kidney diamine oxidase (DAO) and rat intestinal histaminase (Hi-ase) activities are inhibited in vitro by high concentrations of both a substrate (histamine) and a coenzyme (pyridoxal-5'-phosphate). This inhibition may be at least partially associated with the formation of a cyclic compound between histamine (Hi) and pyridoxal-5'-phosphate (PLP). The dynamics of this cyclic compound formation in the presence of both enzymes has been examined. In an incubation mixture containing partially purified pig kidney DAO, the rate of cyclization decreased slightly as compared with a buffer. On the contrary, in the presence of crude rat intestinal histaminase, the rate of cyclization was inhibited significantly; this inhibition was proportional to the amount of enzyme preparation present in the incubation mixture. The possible mechanism of the influence of enzyme protein on the rate of cyclic compound formation, and its possible biological significance, are discussed.

Amine Oxidase (Copper-Containing)↗
PubMed1977

Cholinergic link in the histamine-mediated increase in homovanillic acid in the rat striatum.

Administration of 500 microng of histamine into the lateral brain ventricle of the rat produced a 50% increase in striatal HVA. The DA level remained unchanged. The histamine-mediated elevation of HVA was abolished by pre-treatment with the antihistaminic drug - mepyramine. Moreover atropine significantly reduced the histamine-induced increase of HVA. It is concluded that histamine primarily activates cholinergic neurons and that the changes in DA metabolism are a consequence of an increased cholinergic activity.

Animals↗