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Biomedical subjects

K Magyar

Publications and source records attributed to K Magyar.

At least 73 records · Page 4Linked to original sources
PubMed1989

The asymmetry of 3H-imipramine binding may predict psychiatric illness.

The Bmax and Kd values for 3H-imipramine binding were measured in post-mortem human brains from drug-free selected psychiatric subject homicide victims (n = 15) and normal controls (n = 15). The two groups were comparable in age and gender. The number of imipramine binding sites (Bmax) in the frontal cortices of psychiatric subjects had significantly higher Bmax values in the left hemisphere than in the right hemisphere. Inversely, the number of imipramine binding sites (Bmax) in the frontal cortices of normal controls were significantly higher in the right brain than in the left brain. It was postulated that the inhibiting effect of central serotonin (5-HT) has weakened in psychiatric cases, therefore the change of presynaptic serotonergic activity might be associated with psychiatric illness in the left hemisphere of human brain.

Adolescent↗
PubMed1989

Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells.

1. The spontaneous release of [3H]noradrenaline [( 3H]NA) has been measured from rabbit pulmonary arteries and bovine chromaffin cells in the presence of neuronal uptake blocker cocaine (3 x 10(-5) M). 2. The Na+-pump inhibitor sodium-azide (NaN3, 2mM) produced a moderate increase of [3H]NA release from both preparations and relaxed the arteries. The [3H]releasing action of NaN3 was accompanied by a 30% inhibition of 86Rb-uptake into chromaffin cells. 3. In both preparations, ouabain (10(-4) M) markedly increased the release of [3H], contracted the arteries and inhibited the 86Rb-uptake of chromaffin cells by about 75%. A combined application of NaN3 and ouabain produced a similar inhibition of 86Rb-uptake of chromaffin cells and failed to increase further the release of [3H] in comparison to that found in response to ouabain alone. 4. Removal of K+ from the external medium increased both the release of [3H]NA and the tone of pulmonary arteries. NaN3 further increased the transmitter release in "K+-free" solution but relaxed the muscle. In the absence of external K+ and in the presence of azide, ouabain further enhanced the transmitter release but failed to produce significant contraction. 5. Reactivation of the Na+-pump by readmission of K+ (5.9 mM) to the external medium abolished the transmitter releasing action of NaN3 in arteries. 6. It is concluded that in peripheral sympathetic nerves and chromaffin cells, NaN3 inhibits the Na+-pump producing NA and CA release respectively and in nerves even if NA release had already been increased by K+-removal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A-23187 evoked transmitter release from rabbit pulmonary artery and its inhibition by reactivation of sodium-pump.

1. The spontaneous [3H]-release has been measured from the isolated main pulmonary artery of the rabbit preloaded with [3H]noradrenaline in the presence of uptake blockers (cocaine, 3 x 10(-5) M; corticosterone, 5 x 10(-5) M). 2. The Ca-ionophore A-23187 (3 x 10(-7)-3 x 10(-5) M) increased the outflow of [3H] by a concentration dependent manner. 3. Inhibition of Na+-pump by removal of K+ from the external medium also increased the release of labelled noradrenaline. 4. In the absence of external K+, the applied A-23187 (3 x 10(-6) M; EC50) further increased the release of [3H]. 5. Reactivation of Na+-pump by readmission of K+ (5.9 mM) to the external medium abolished the [3H]-release which had previously been increased in "K+-free" solution. 6. The reactivated Na+-pump significantly inhibited the transmitter releasing action of A-23187. 7. This latter was antagonized by an increase of external Ca2+ (7.5 mM). 8. It is concluded that the reactivated Na+-pump caused re-establishment of Na+-gradient is capable to counteract the Ca-ionophore facilitated Ca2+-influx and release from internal stores, which can be antagonized by excess Ca2+.

Animals↗
PubMed1989

Prostacyclin mediates antiaggregatory and hypotensive actions of endothelin in anaesthetized beagle dogs.

The effects of endothelin on blood pressure and in vivo aggregation of platelets were studied in anaesthetized beagle dogs. Intravenous administration of endothelin (0.03-0.3 nmol kg-1) resulted in a dose-dependent transient hypotension followed by a long-lasting hypertension and inhibition of platelet aggregation. These changes were accompanied by dose-dependent elevation of plasma 6-keto prostaglandin F1 alpha levels. Pretreatment of the animals with acetylsalicylic acid significantly attenuated both the vascular and antiaggregatory responses to endothelin. These data provide evidence for in vivo release of prostacyclin by endothelin in anaesthetized dogs.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Altered responsiveness of diabetic dog renal arteries to acetylcholine and phenylephrine: role of endothelium.

The mechanical responses to acetylcholine (ACh), sodium nitroprusside and phenylephrine (PE) were determined in normal and diabetic dog renal arterial strips with and without endothelium. Experimental diabetes increased the sensitivity, IC50 = (2.9 +/- 0.4) X 10(-8) mol/l in normal and (9.6 +/- 1.5) X 10(-9) mol/l in diabetic (p less than 0.01, n = 6) to ACh of endothelium intact renal arterial strips without influencing the maximum relaxation induced by this agonist. In all intact vessels PE produced contractions of equal magnitude. Removal of the endothelium completely abolished the relaxant ability of ACh, and caused a slight increase in the contractile response of both diabetic and normal strips to PE. The maximum contractile force generated by the denuded diabetic vessels in response to PE was significantly (p less than 0.01) greater than the maximum tension produced by the denuded nondiabetic arteries. The sensitivity of the tissues to PE was, however, not modified by either diabetes or endothelium removal. The direct relaxant sodium nitroprusside elicited a similar degree of relaxation in the two groups of arteries. Cyclooxygenase blockade had no effect on either the relaxation or contractile responses of any of the preparations. These findings suggest that short-term diabetes makes dog renal arteries supersensitive to ACh and hyperreactive to PE.

Acetylcholine↗
PubMed1988

Effect of adjuvant reserpine treatment on catecholamine metabolism in schizophrenic patients under long-term neuroleptic treatment.

The clinical and biochemical effects of adjuvant reserpine treatment were investigated in 12 chronic schizophrenic patients on long-term neuroleptic medication. The global severity of the symptoms using the Brief Psychiatric Rating Scale did not change significantly in the whole group, however, a moderate decrease in positive symptoms (factors though disturbance, activation and hostile-suspiciousness) was observed for 5 patients. Cerebrospinal fluid (CSF) noradrenaline levels showed a consistent decrease, but other biochemical parameters (CSF dopamine metabolites, platelet MAO and serum dopamine-beta-hydroxylase activities) did not change significantly. The changes of clinical symptoms and biochemical parameters did not show any correlation.

Adjuvants, Pharmaceutic↗
PubMed1988

Influence of experimental diabetes on the mechanical responses of canine coronary arteries: role of endothelium.

The influence of experimental diabetes on the endothelium mediated relaxation and contractile responses of canine isolated coronary arteries was studied in arteries removed from alloxan treated diabetic (280 mmol.kg-1) and control mongrel dogs. Strips with and without endothelium were suspended in Krebs bicarbonate solution for isometric recording. Relaxation responses to acetylcholine (1.8 X 10(-8) to 9.4 X 10(-6) mol.litre-1, A23187 (10(-8) to 1.28 X 10(-6) mol.litre-1), and sodium nitroprusside (10(-9) to 10(-7) mol.litre-1) as well as contractile responses to prostaglandin F2 alpha, (1.7 X 10(-7) to 5.6 X 10(-4) mol.litre-1) were determined. In all intact strips acetylcholine, and A23187 induced similar concentration dependent reduction of the prostaglandin F2 alpha (2 X 10(-6) mol.litre-1) evoked tone. No significant difference was observed between sodium nitroprusside evoked relaxations of normal and diabetic arteries. Cyclooxygenase blockade reduced the maximal relaxations induced by acetylcholine and A23187 in diabetic vessels, whereas it did not change the endothelium dependent relaxation of normal arteries. Diabetes increased significantly the sensitivity to acetylcholine (EC50 4.1(0.4) X 10(-7) mol.litre-1 in control and 6(0.7) X 10(-8) mol.litre-1 in diabetic arteries; p less than 0.01, n = 7) and to A23187 (EC50: 7(1) X 10(-8) mol.litre-1 in control and 3.8(0.3) X 10(-8) mol.litre-1 in diabetic vessels; p less than 0.01, n = 7); in contrast, prostaglandin F2 alpha remained an equiactive constrictor in normal and diabetic vessels with intact endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1988

Effects of PGI2, CH-7284 and CH-7384 on spontaneous platelet aggregation and blood pressure of anaesthetized beagles.

Chinoin-7284 and Chinoin-7384 are chemically stable derivatives of prostacyclin. We compared the hypotensive and antiaggregatory effects of PGI2 and the two analogues using our computerized aggregometric system. The in vivo antiaggregatory activity was measured with a modified filtration pressure technique in anaesthetized beagle dogs: The change in arterial blood pressure was measured simultaneously. The dose-response relationship and the duration of action of prostacyclin and their analogues following bolus administration have been determined. The molar dose of PGI2, CH-7284 and CH-7384 that produced 25 mmHg reduction in filtration pressure were 0.3 +/- 0.06 nmol/kg; 7.37 +/- 0.94 nmol/kg; 17.19 +/- 1.76 nmol/kg respectively (n = 6). The molar doses that produced the same decrease in mean arterial pressure were 0.61 +/- 0.06 nmol/kg; 15.59 +/- 4.73 nmol/kg; 21.05 +/- 7.20 nmol/kg respectively (n = 6). There were no significant differences between equipotent doses of prostacyclin and its analogues with respect to the duration of antiaggregatory and hypotensive action. The in vivo selectivity ratios (hypotensive potency/antiaggregatory potency) of PGI2, CH-7284 and CH-7384 were 0.49, 0.47 and 0.85 respectively. The results indicate that these two PGI2 analogues have the same character as regards the in vivo duration of actions and in vivo selectivity, as has the parent compound.

Animals↗
PubMed1988

In vivo antiaggregatory effect of BM 13.177 on the spontaneous platelet aggregation in anaesthetized beagle dogs.

The arterial blood of anaesthetized heparin-treated beagle dogs was directed through a 30/um diameter pore size screen by a roller pump at a constant rate. As a result, the pressure proximal to the filter continuously increased. The filtration pressure stabilizing concentration of prostacyclin (infused proximal to the filter) was determined. BM 13.177 -similar to PGI2- was able to slow down and stop the increase of filtration pressure (final conc.: 1-10/uM). In addition it could reverse the filter occlusion process. The lowest concentration of BM 13.177 (0.1-1/uM) did not affect significantly the filter occlusion rate, but it markedly enhanced the antiaggregatory effect of PGI2 when these drugs were administered simultaneously. In summary, we can conclude that 1) generation of thromboxane and endoperoxide plays a key role in the mechanism of the spontaneous platelet aggregation on the filter; 2) BM 13.177 significantly potentiates the antiaggregatory effect of PGI2 in vivo.

Animals↗