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Biomedical subjects

M Koltai

Publications and source records attributed to M Koltai.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Obstetric analgesia using nitralgin inhalation and lumbal peridural anesthesia (a model for obstetric analgesia)].

Authors report the systems of anesthesia used at their ward for delivery in the last eight years. Nitralgin inhalation is used since 1981, lumbar peridural anesthesia is used since 1983. Of 13,458 deliveries in case of 3893 parturiants Nitralgin analgesia was used, while LEDA was used for 2300 parturients. By means of Nitralgin inhalation system it could be assured in the delivery room to apply the pain relief gas mixture (Nitralgin) simultaneously for several parturients. With direction of anesthesiologists employed for the ward the LEDA was attained by gynecologists knowing the use and application of general anesthesia. Thus the continuous application of both procedures can be ensured in 24 hours a day. In our study the frequency of vacuum extraction (0.26 p. c.) and that of Cesarean section (12.81 p. c.) did not increase. With application of these methods it could be achieved that 60 p. c. of vaginal deliveries are performed with anesthesia. Authors propose their system for wider application since in the same ward more and more parturients can be applied anesthesia for pain relief at vaginal delivery.

Adult↗
PubMed1990

Dexamethasone treatment attenuates the development of ischaemic brain oedema in gerbils.

Transient global forebrain ischaemia was produced in Mongolian gerbils by occluding both common carotid arteries for 10 min followed by 48 h recirculation. Dexamethasone, 5 mg/kg i.p., was given 5 h before the occlusion and every 12 h thereafter. After occlusion an increase in water, sodium and calcium content was found in the parietal cortex and hippocampus, while the concentration of potassium decreased. Exudation of plasma albumin was not found in the brain. The activity of Na+, K(+)-ATPase decreased in the hippocampus. Morphological signs of cerebral oedema were also observed, both in the CA1 region of the hippocampus and in the cortex. Dexamethasone treatment prevented the accumulation of water, sodium and calcium in the ischaemic brain. It also attenuated the oedematous morphological changes of the blood-brain barrier. Thus dexamethasone treatment may also have therapeutic relevance in the acute, high-risk phase of patients suffering from repetitive, transitoric cerebral ischaemia.

Animals↗
PubMed1990

Effect of cicletanine on reperfusion-induced arrhythmias and ion shifts in isolated rat hearts.

Isolated hearts from normotensive (NT) and spontaneously hypertensive (SH) rats, subjected to normothermic global ischemia, were used to study whether cicletanine (a new antihypertensive drug) treatment exerts an antiarrhythmic effect against reperfusion-induced arrhythmias. The effect of the drug on myocardial ion contents (Na+, K+, Ca2+, and Mg2+) during ischemia and reperfusion was also determined. Using the optimal doses of cicletanine (30 and 100 mg/kg orally for 14 days), the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT) was reduced from their control values of 91 and 100% (after 30 min of ischemia) to 41 (p less than 0.05), 50 (p less than 0.05) and 41 (p less than 0.05), 58% in the NT group, while the corresponding value in the SH group for VF and VT were 17 (p less than 0.001), 33 (p less than 0.01) and 17 (p less than 0.001), 25% (p less than 0.001), respectively. The results obtained indicate that the cardioprotective effect of cicletanine was greater in the SH group than in the NT group. Cicletanine significantly reduced the ischemia- and reperfusion-induced myocardial Na+ and Ca2+ gains and inhibited the loss of myocardial K+ and Mg2+ in both NT and SH groups. The antiarrhythmic effect of cicletanine appears to be correlated with the preservation of myocardial Na+, K+, Ca2+, and Mg2+ contents via an ion transport modulation.

Animals↗
PubMed1989

Inhibition by H-7 of the protein kinase C prevents formation of brain edema in Sprague-Dawley CFY rats.

The effect of the protein kinase C enzyme inhibitor H-7 was examined on the brain edema formation evoked by bilateral occlusion of the common carotid arteries in Sprague-Dawley rats of CFY strain. Brain edema was assessed by measurement of water and electrolyte contents of the brain. The results showed that pretreatment with H-7 reduced the extent of brain edema formation in a dose-dependent manner. The fact that H-7 treatment prevented the accumulation of water and certain electrolytes in the brain indicates that the protein kinase C may be activated not only in the neuronal structures but also in the microvessels during ischemia, which can lead directly or via certain calcium-mediated mechanisms to the opening of tight junctions resulting in the development of brain edema.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Ginkgolide B protects isolated hearts against arrhythmias induced by ischemia but not reperfusion.

The effect of ginkgolide B (BN 52021), a specific platelet-activating factor (PAF) antagonist, applied in doses of 1.5, 3.0, 6.0 X 10(-5) and 1.2 X 10(-4) mol/l, in comparison to that of metoprolol (10(-5) mol/l) and diltiazem (10(-7) mol/l), two widely used antiarrhythmic agents, on ischemia- and reperfusion-induced arrhythmias and heart functions, such as heart rate (HR), coronary flow (CF), aortic flow (AF), left ventricular developed pressure (LVDP), its first derivative (LVdp/dtmax), and left ventricular end-diastolic pressure (LVEDP) in isolated working rat hearts was examined. BN 52021 caused a dose-related protection against dysrhythmias, such as ventricular fibrillation, ventricular tachycardia, and premature ventricular beats induced by ischemia (30 min ligation of the left anterior descending coronary artery). The antiarrhythmic effect of BN 52021 given in a dose of 6.0 X 10(-5) mol/l was comparable to that of diltiazem and superior to the activity of metoprolol. None of the drugs influenced reperfusion-induced rhythm disturbances. BN 52021 did not alter heart functions, while metoprolol reduced (LVEDP only, and diltiazem increased CF, decreased AF, LVDP, and LVdp/dtmax during regional ischemia, indicating a negative inotropic effect. The antiarrhythmic effect of BN 52021 appears to be related to an antagonism of an increase in slow calcium influx induced by PAF in myocardial cells. Similarly to the mechanism of action of established antiarrhythmic drugs, BN 52021 can presumably prevent the re-entry mechanism involved in the development of ischemia-induced rhythm disturbances.

Animals↗
PubMed1989

Is there a case for PAF antagonists in the treatment of ischemic states?

It is becoming clear that PAF plays an important role in a variety of life-threatening pathologies including shock, asthma, graft rejection and ischemia-induced damage. Pierre Braquet and colleagues analyse recent reports on PAF and ischemia and propose a hypothesis based on the catastrophe theory to explain why PAF antagonists are effective in countering ischemic injury and many other disorders. PAF antagonists, perhaps in combination with other agents, may consequently prove to have extensive therapeutic potential.

Humans↗
PubMed1989

Effects of low extracellular sodium concentration on reperfusion induced arrhythmias: changes in the myocardial sodium, potassium and calcium contents in isolated guinea pig hearts.

Isolated guinea pig hearts subjected to global ischaemia were used to investigate whether low extracellular Na+ exerts an anti-arrhythmic action against reperfusion arrhythmias, and the effects of extracellular Na+ manipulation upon myocardial ion contents (Na+, K+ and Ca2+) during ischaemia and reperfusion were studied. Using an optimal concentration of 144 mmol.litre-1 of extracellular Na+, hearts were subjected to 10, 20, 25, 30 or 40 min of global ischaemia followed by 25 min reperfusion. A bell shaped curve was obtained such that with increasing durations of ischaemia from 20 to 30 min there was an increasing incidence of reperfusion arrhythmias. Beyond this optimum (at which 100% exhibited reperfusion induced ventricular fibrillation and tachycardia) there was a decline in the susceptibility of the hearts to arrhythmias. Low extracellular Na+ was given 5 min prior to the global ischaemia and maintained during reperfusion. With extracellular Na+ of 24, 54, 84 and 114 mmol.litre-1, reperfusion induced ventricular fibrillation and tachycardia were reduced from their control incidence of 91% and 100% to 8% (p less than 0.001) and 17% (p less than 0.001), 17% (p less than 0.01) and 17% (p less than 0.001), 41% (p less than 0.05) and 50% (p less than 0.05), and 91% and 91%, respectively. Both ischaemia induced Na+ gain and K+ loss were inhibited by low extracellular Na+ (24 mmol.litre-1). During reperfusion, myocardial Na+ was further increased in the control group and this value was lower in the low extracellular Na+ group. In control hearts, myocardial K+ was suddenly increased during the first 5 min of reperfusion, then continuously decreased until the end of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Possible involvement of platelet activating factor in anaphylaxis of passively sensitised, isolated guinea pig hearts.

There is evidence that cardiac tissue may be a target for antigen/antibody reactions. Platelet activating factor (PAF) is released during anaphylaxis and could mediate cardiac damage. To investigate this, guinea pigs were passively sensitised by anti-ovalbumin rabbit serum (6 mg.kg-1 intravenously) and 24 h later their hearts were excised and isolated according to a working heart preparation technique. After a 20 min equilibration period, anaphylactic challenge was induced by a bolus injection of ovalbumin (2 mg in 0.2 ml buffer) via the side arm of the aortic cannula. Heart rate, coronary flow, aortic flow, left ventricular developed pressure (LVDP), its first derivative (LVdp/dtmax) and left ventricular end diastolic pressure (LVEDP) were recorded. After ovalbumin challenge, heart rate and LVEDP were markedly increased, while coronary flow, aortic flow, LVDP, and LVdp/dtmax were profoundly decreased. All these alterations were over within 5 min, and the measured variables returned to approximately the pre-challenge values. BN 52021, a specific PAF receptor antagonist, was dissolved in the perfusion buffer and given in doses of 15, 30 and 60 mumol.litre-1 10 min prior to the induction of anaphylactic challenge until the end of the observation period. BN 52021 inhibited the increase in heart rate and LVEDP and the decrease in coronary and aortic flow, LVDP and LVdp/dtmax in a dose dependent manner. The changes produced by 30 and 60 mumol.litre-1 were statistically significant at the levels of p less than 0.01 and p less than 0.001 when compared to the control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗
PubMed1989

Effect of the platelet-activating factor antagonist BN 52021 on human natural killer cell cytotoxicity.

The possible role of platelet-activating factor (PAF) in natural killer (NK) cell cytotoxicity was investigated by examining the effect of the PAF antagonist BN 52021 in NK cytotoxicity towards 51Cr-labelled K 562 target cells. When BN 52021 (30-120 microM) was added during the assay, a dose-dependent inhibition of NK activity was observed. The inhibition of cytotoxicity by BN 52021 was not due to an alteration of the binding of lymphocytes to K 562 cells. When lymphocytes were preincubated with BN 52021 (60 microM) for 60 min before the target cells were added, the inhibitory effect of the drug was similar to that observed when it was added at the start of the reaction. Inhibition was more pronounced when the target cells were pretreated for 60 min before the start of the assay. BN 52021 (60 microM) also inhibited gamma interferon induced NK activity. These studies provide indirect evidence that NK cells can generate PAF and that this mediator is involved in cytotoxic processes.

Cytotoxicity, Immunologic↗
PubMed1989

[Effect of cicletanine on arrhythmia and intracellular sodium accumulation in the isolated rat heart during ischemia and reperfusion].

The antiarrhythmic effects of cicletanine (CIC), a new antihypertensive drug, were studied on isolated hearts from SHR and WKY rats subjected to global normothermic ischaemia. The effects of CIC on variations in intracellular sodium concentration induced by ischaemia-reperfusion were measured. After a 14-day treatment with CIC in doses of 30 and 100 mg/kg/day, the results were as follows: in WKY rats the incidence of ventricular fibrillation (VF) was reduced from 91% in controls to 41% and 50% (p less than 0.05) and the incidence of ventricular tachycardia (VT) was reduced from 100% to 41% and 58% (p less than 0.05). In SHR rats the percentages of VF were 100% in controls and 17% (p less than 0.001) and 33% (p less than 0.01) respectively in treated animals. Similarly, the incidence of VT was reduced from 100% to 17% (p less than 0.001) and 25% (p less than 0.001) respectively. The effects of CIC were more pronounced on SHR rats than on WKY rats. CIC reduced the intracellular sodium accumulation induced by ischaemia and reperfusion. The antiarrhythmic activity of CIC seems to be correlated with its inhibitory activity on intracellular sodium accumulation.

Animals↗
PubMed1989

Antimicrobial and immunomodulating effects of some phenolic glycosides.

Several phenolic glycosides, i.e. acteoside, desrhamnosyl acteoside, and purpureaside A, B and C, exerted weak antibacterial effects on Escherichia coli. Acteoside had antiplasmid effects, including F'lac plasmid elimination, and inhibited kanamycin resistance transfer in E. coli. Acteoside, desrhamnosyl acteoside and purpureaside A displayed antiviral effect on Aujeszky virus. All of the phenolic glycosides decreased some human leucocyte functions, including rosette formation, mitogen-induced blast transformation and phagocytic activity in vitro. The purpureaside C had significant proinflammatory action, however, other phenolic glycosides showed neither proinflammatory nor antiinflammatory effect on carrageenin-induced inflammation in vivo.

Animals↗
PubMed1989

The effect of the platelet-activating factor antagonist, BN 52021, on human natural killer cell-mediated cytotoxicity.

The influence of the platelet-activating factor (PAF) antagonist, BN 52021, on human natural killer (NK) cell cytotoxicity against K 562 target cells was determined. Cytotoxicity was measured by a short-term (4 hr) 51Cr-release assay. The cytotoxicity was significantly reduced in the presence of PAF antagonist at concentrations from 30 to 120 microM. This reduction of killing was not due to the impairment of binding of effector cells to target cells. Pretreatment of K 562 target cells with the PAF antagonist led to a greater inhibition of NK cell cytotoxicity compared with that observed when the effector cells were preincubated with BN 52021. Thus, the inhibition of cytotoxicity appears to be due to an effect of BN 52021 on target cells rather than on lymphocytes. Furthermore, the increase in NK activity induced by interferon was less pronounced when BN 52021 was added in the incubation medium. The natural cytotoxicity of platelet-depleted or large granular lymphocyte-enriched effector cell populations was inhibited by the PAF antagonist in a similar manner. The effect of BN 52021 appears to be related to its specific PAF antagonistic activity since a similar action on NK cells was noted with two other structurally unrelated PAF antagonists, BN 52111 and WEB 2086. In contrast, Ginkgolide J (BN 52024), which is structurally related to BN 52021 but lacks PAF antagonistic activity, was ineffective in inhibiting NK cell cytotoxicity. Finally, synthetic PAF induces a dose-dependent cytotoxic action on K 562 cells and this effect of the autacoid is inhibited by BN 52021. These observations provide indirect evidence that PAF could play a role in the mechanism(s) of NK cytotoxity.

Cells, Cultured↗
PubMed1988

Beta-adrenergic receptors of lymphocytes in children with allergic respiratory diseases.

The beta-adrenergic receptor binding sites on peripheral lymphocytes in children with bronchial asthma (n = 16) and seasonal allergic rhinitis (n = 8) were examined in comparison with normal controls (n = 18) by means of 124I-cyanopindolol. The number of beta-adrenergic receptors was significantly lower in the asthmatic group (858 +/- 460/lymphocyte) than in the controls (1564 +/- 983/lymphocyte). The value (1891 +/- 1502/lymphocyte in children with allergic rhinitis was slightly higher than that in healthy controls. Of the 24 patients suffering from allergic diseases of the lower or upper airways, the bronchial histamine provocation test was performed in 21; 16 gave positive results, while 5 were negative. No difference in beta-adrenergic receptor count was found between the histamine-positive and negative patients. Neither was there any correlation between the number of beta-adrenergic receptors and the high (16/24) and low (8/24) serum IgE concentrations found in allergic patients. The significant decrease in beta-adrenergic receptor count in asthmatic children lends support to Szentiványi's concept. Further qualitative and quantitative analysis of lymphocyte beta-adrenergic receptors may provide an individual approach to the treatment of bronchial asthma with beta-sympathomimetic drugs.

Adrenergic beta-Antagonists↗
PubMed1987

Glucocorticoid-induced low molecular mass anti-inflammatory factors which do not inhibit phospholipase A2.

The peritoneal lavage fluid of dexamethasone (DXM)-pretreated rats was filtered through an Amicon YM-10 membrane (cutsize 10 kD). The retentate inhibited dextran oedema. Its 40 kD fraction (lipocortin) obtained by molecular sieving on Sephadex (SG)-75, suppressed carrageenin-induced foot swelling and phospholipase A2 (PLA2) activity, but it had no effect on the dextran response. The Amicon filtrate was chromatographed on SG-25 gel and yielded 6 and 2 kD fractions suppressing dextran and serotonin (5-HT) oedema but not carrageenin inflammation and PLA2 activity. These fractions may be active fragments of vasocortin, a glucocorticoid-induced mediator regulating vascular permeability.

Adrenalectomy↗
PubMed1986

Effect of BN 52021, a specific PAF-acether antagonist, on cardiac anaphylaxis in Langendorff hearts isolated from passively sensitized guinea-pigs.

Hartley guinea-pigs were sensitized passively with antiovalbumin rabbit serum. Their isolated perfused hearts responded to the specific antigen with a marked decrease in contractile force, increase in perfusion pressure, and rhythm disturbances. All these impairments except tachycardia were decreased by BN 52021, a specific PAF-acether receptor antagonist, applied in a constant infusion before ovalbumin challenge. These findings suggest that PAF-acether plays a major role as mediator in cardiac anaphylaxis, and BN 52021 may be a valuable therapeutic agent in allergic conditions.

Anaphylaxis↗
PubMed1986

Effects of dexamethasone on brain edema induced by kainic acid seizures.

The histopathological alterations developing in the hippocampus, piriform cortex and thalamus of the rat brain, the blood-brain barrier damage, and the effects of dexamethasone pretreatment on the brain edema were investigated 4 h following intraperitoneal kainic acid administration. The most pronounced Evans Blue extravasation accompanied by increases in the water and sodium contents and a decrease in the potassium content, were observed in the thalamus. Dexamethasone, injected in a dose of 5 mg/kg 2 h before kainic acid administration, reduced considerably the vasogenic edema and neuronal damage in the thalamus, but the cytotoxic edema of the hippocampus and piriform cortex remained unaltered. Kainic acid-induced seizures lead to the development of vasogenic brain edema mainly in the thalamus, as well as to cytotoxic edema in the hippocampus and piriform cortex. The vasogenic edema seems to contribute to the cell damage in the thalamus. Dexamethasone reduces the vasogenic edema and cell damage in the thalamus, possibly by inducing the synthesis of certain protein(s) with antiphospholipase A2 activity.

Animals↗