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Biomedical subjects

K Magyar

Publications and source records attributed to K Magyar.

At least 127 records · Page 7Linked to original sources
PubMed1983

Effects of indomethacin and prostaglandins I2 and E2 on the tone of human isolated mesenteric arteries.

The actions of indomethacin (IND), PGE2 and PGI2 were studied on the tone of isolated mesenteric arteries obtained from operated patients. The cyclooxygenase inhibitors IND (3 mumol/l) and suprofen (0.58 mumol/l) increased the resting tone and potentiated the contractile responses to electrical stimulation and noradrenaline. Low concentrations of PGE2 (0.7-5.6 X 10(-9) mol/l) decreased the baseline tone and reduced the stimulation-evoked contractions whereas higher concentrations (from 5.7 X 10(-8) mol/l) increased the tone of vessels. PGI2 (0.7-10.8 X 10(-9) mol/l) also relaxed IND-treated arteries but, in contrast to PGE2, it did not produce contraction even at a concentration of 10(-6) mol/l. Prostacyclin reduced the tone evoked and sustained by a high concentration of PGE2 or PGF2 alpha, the IC50 values being 46.2 or 7.9 X 10(-9) mol/l, respectively. The contractile responses to electrical stimulation and to noradrenaline were also inhibited by PGI2 (IC50 5.6 and 6.8 X 10(-9) mol/l, respectively). These results suggest that the smooth muscle cells of human mesenteric arteries are just as sensitive to IND, PGE2 and PGI2 as are those from laboratory animals. Our observations may be of clinical importance.

Adult↗
PubMed1982

Stimulation by vanadate of [3H]noradrenaline release from rabbit pulmonary artery and its inhibition by noradrenaline.

Vanadate, the +5 oxidation state of vanadium, present in mammalian tissues, even in nerve tissue, and a competitive inhibitor of NaK-ATPase, significantly enhanced the release of [3H]noradrenaline evoked from rabbit isolated perfused pulmonary artery by electrical stimulation. Its effect proved to be concentration-dependent. Noradrenaline (10(-6) M) reduced the vanadate-potentiated release of [3H]noradrenaline. The effect of noradrenaline is mediated via alpha 2-adrenoceptors as evidenced by the finding that yohimbine 3 x 10(-7) M prevented its action. The effect of vanadate was dependent on external K ions. When the effect of vanadate on [3H]noradrenaline release was studied under conditions when the NaK-ATPase enzyme activity was inhibited by removal of external K for 45 min, vanadate was ineffective. This finding indicates that the effect is related to the inhibition of NaK-ATPase activity, a condition known to result in transmitter release.

Adrenergic alpha-Agonists↗
PubMed1982

Nanomolar concentrations of prostaglandin F2 alpha potentiate cholinergic contractions of rabbit isolated tracheal muscle.

The effects of prostaglandin F2 alpha (PGF2 alpha) on stimulation- or acetylcholine-evoked contractions were studied in isolated airway muscle preparations from rabbits, guinea-pigs and humans. Low concentrations of PGF2 alpha (10(-9) to 9 X 10(-8) mol/1) produced a dose-related (10-300%) increase in the contractile responses of the rabbit trachealis muscle to electrical stimulation at 2 Hz. This effect was inversely related to the rate of stimulation. In seven out of forty two preparations the resting muscle tone was also increased by 1.1 X 10(-8) mol/1 or higher concentrations of PGF2 alpha. This substance enhanced the contractile responses to acetylcholine (1-2.7 X 10(-8) mol/1) to the same extent as those to electrical stimulation. The potentiation produced by PGF2 alpha was not affected by indomethacin, mepyramine, methysergide or phenoxybenzamine. Electrically evoked contractions of isolated tracheal strips of guinea-pig or segments of human bronchial muscles were not changed significantly in the presence of 0.1-5 X 10(-8) mol/1 of PGF2 alpha. These results suggest that PGF2 alpha may modulate airway muscle tone by enhancing the postsynaptic stimulatory effect of acetylcholine released from the pulmonary cholinergic nerve endings. This modulation seems to be species-dependent.

Acetylcholine↗
PubMed1982

Relaxation by prostacyclin (PGI2) and 7-oxo-PGI2 of isolated cerebral, coronary and mesenteric arteries.

The relaxant effects of prostacyclin (PGI2) and its stable 7-oxo-analogue, a product of Chinoin Pharmaceutical Works, were compared on isolated canine cerebral, bovine coronary, rabbit coeliac and human mesenteric arterial strips. The resting tone of the coronary, cerebral and human mesenteric arteries as well as the stimulation- or noradrenaline-evoked tone of coeliac vessels were reduced by both prostanoids. The relaxant action of 7-oxo-PGI2 was slow in onset and lasted until it was washed out. The IC50 values were 4 to 40 X 10(-9) mol/l for PGI2 and 1 to 6 X 10(-7) mol/L for 7-oxo-PGI2. Compared to PGI2, 7-oxo-PGI2 was more potent in relaxing coronary arteries than the other vessels studied. Isolated tracheae from guinea-pigs were contracted by PGI2 while relaxed by 7-oxo-PGI2.

Animals↗
PubMed1981

Evidence that morphine and opioid peptides do not share a common pathway with adenosine in inhibiting acetylcholine release from isolated intestine.

1 The release of acetylcholine from guinea-pig ileal isolated longitudinal muscle strip with intact Auerbach's plexus was measured by bioassay and by a radioisotope technique. 2 Normorphine (5 x 10(-7)M) and D-Met2, Pro5-enkephalinamide (D-Met, Pro-EA) reduced the release of acetylcholine. Theophylline, an adenosine antagonist, failed to prevent the inhibitory effect of normorphine or D-Met, Pro-EA. 3 Theophylline (1.7 x 10(-4)M) by itself enhanced the twitch responses to field stimulation (0.1 Hz) but did not prevent the inhibitory effect of normorphine and D-Met, Pro-EA. 4 From the results it can be concluded that morphine and opioid peptides do not share a common pathway with adenosine in inhibiting acetylcholine release from axon terminals of Auerbach's plexus.

Acetylcholine↗
PubMed1981

The fate of p-bromo-methylamphetamine (V-111) in the body.

The fate of p-bromo-methylamphetamine (V-111) in the body was studied by means of its radioactive labelled forms in mouse and rat experiments. It was found with the whole body autoradiographic method and liquid-scintillation measurements that the compound is rapidly absorbed by whatever routes of administration and it is rapidly taken up by the tissues from the blood stream. In the central nervous system, it reaches higher concentration than methyl-amphetamine and it leaves the central nervous system more slowly. We have shown with differential centrifugation that V-111 is bound much more avidly to the mitochondrial and microsomal fractions of rat brain than methyl-amphetamine and o-bromo-methyl-amphetamine (V-104). The intensity of binding is proportional to the lipid solubility of the compounds. V-111 and its metabolites are excreted mainly in the urine, and they can be found in small amounts also in the stool. In the case of V-111-3-14C a small amount of 14CO2 appeared in the expired air, too, which is a consequence of the disintegration of the molecule. It has been shown by the radiochromatographic and gas chromatographic, mass-spectrometric analysis of the metabolites that V-111 is excreted partly in unchanged form, nevertheless, the N-demethylated and subsequent products, viz. p-bromo-phenyl-acetone, p-bromo-phenylpropanol, p-bromo-benzoic acid and p-bromo-hyppuric acid are also excreted in the urine. The main metabolic pathway of amphetamine and of its methyl-derivative in rat is p-hydroxylation, which does not take place in the case of p-halogenated V-111. Thus the secondary metabolic pathway (demethylation, oxidative desamination) becomes the main metabolic route of V-111 in this species. The vigorous demethylation of V-111 was proved both in vivo and in vitro. In the rat, demethylating activity increases during prolonged treatment. The latter fact has to be taken into consideration when interpreting the pharmacological tolerance that develops during chronic administration of the compound.

Absorption↗
PubMed1980

The role of metabolic factors in the interaction between opiates and homopyrimidazoles in the central nervous system.

Both the analgesic and the antitussive effects of morphine, codeine and azidomorphine, azidocodeine and azidoethylmorphine are potentiated in rats and cats by Probon, a minor analgesic, with a homopyrimidazole structure. The analgesic effect of opiates and their toxicity are more strongly influenced by the N-methylhomopyrimidazoles than their antitussive effect. In the potentiation between Probon and morphine derivatives metabolic interference may play a role at the N-demethylation level, occuring in the liver microsomes.

Analgesics↗