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1.

001-es BibID:BIBFORM041630
035-os BibID:PMID:3557105
Első szerző:Blasig, Ingolf E.
Cím:Effect of activated oxygen species on mitochondria isolated from myocardium after reperfusion injury / I. E. Blasig, P. Bor, A. Tósaki, L. Szekeres, H. Löwe
Dátum:1986
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Physiol biophys 5 : 6 (1986), p. 655-658. -
További szerzők:Bor P. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szekeres László Löwe, H.
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2.

001-es BibID:BIBFORM041627
035-os BibID:PMID:2938453
Első szerző:Koltai Mátyás
Cím:Glucocorticoids in myocardial and cerebral infarction / M. Koltai, Á. Tósaki, I. Leprán, L. Szekeres
Dátum:1986
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Agents and Actions 17 : 3-4 (1986), p. 278-283. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Leprán István Szekeres László
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3.

001-es BibID:BIBFORM041626
035-os BibID:PMID:6548971
Első szerző:Koltai Mátyás
Cím:Prevention by macrocortin of global cerebral ischemia in Sprague-Dawley rats / Mátyás Koltai, Árpád Tósaki, Géza Adám, Ferenc Joó, György Nemecz, László Szekeres
Dátum:1984
Megjegyzések:We have previously shown that dexamethasone protects female Sprague-Dawley CFY rats against global cerebral ischemia induced by bilateral carotid artery ligation. In the present study, macrocortin derived from rat peritoneal cells exposed to dexamethasone was found to exhibit antiphospholipase A2 activity and to provide significant protection against the fatal consequences of carotid artery ligation. These results suggest that the cerebroprotective effect of glucocorticoids may be related to macrocortin production.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Pharmacology 105 : 3-4 (1984), p. 347-350. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Ádám Géza Joó Ferenc (1949-) (vegyész) Nemecz György Szekeres László
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4.

001-es BibID:BIBFORM042097
Első szerző:Szekeres László
Cím:Release of 6-keto-PGF1 alpha and thromboxane B2 in late appearing cardioprotection induced by the stable PGI analogue : 7-OXO-PGI / Szekeres László, Tósaki Árpád
Dátum:1993
Megjegyzések:We have shown earlier that prostacyclin (PGI2) and its stable analogue: 7-oxo-prostacyclin(7-OXO) may induce a prolonged, late appearing (24-48 h after drug administration), dose dependent protection of the heart from harmful consequences of a subsequent severe ischaemic stress, such as myocardial ischaemia, life-threatening ventricular arrhythmias and early ischaemic morphological changes. In an other study we observed that a similar but shortlived (less than 1 h) cardioprotection, induced by 'preconditioning' brief coronary artery occlusions, is greatly reduced by blockade of the cyclooxygenase pathway, suggesting that prostanoids might play a role in this shortlasting protection. Objective of our present study was to elucidate the importance of some arachidonic acid (AA) metabolites, such as PGI2 and thromboxane A2 (TXA2) in the mechanism of the late appearing, prolonged cardioprotection. Estimation of the metabolites: 6-keto-PGF1 alpha (6-KETO) and thromboxane B2 (TXB2) was made from the perfusate of isolated Langendorff hearts of guinea-pigs pretreated with 50 micrograms/kg 7-OXO, 24 and 48 h before preparation. Pretreatment alone produced a slight, but significant elevation of 6-KETO (from 206 +/- 11 to 284 +/- 19 pg/ml/min after 24 h, and to 261 +/- 18 pg/ml/min after 48 h). No change was seen in TXB2 production. Global ischaemia for 25 min (followed by 25 min reperfusion) markedly increased the release of both AA metabolites; maximal values were observed in the third min of reperfusion (6-KETO from 206 +/- 11 to 1275 +/- 55 pg/ml/min and TXB2 from 29 +/- 4 to 172 +/- 12 pg/ml/min)
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular and Cellular Biochemistry 119 : 1-2 (1993), p. 129-132. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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5.

001-es BibID:BIBFORM041656
Első szerző:Szekeres László
Cím:Delayed protection by oxo-7-PGI2 against cardiac transmembrance ion shipfts and early morphological changes due to ischemia and reperfusion / Szekeres L., Bálint Zs., Karcsu S., Tósaki A.
Dátum:1990
Megjegyzések:In previous experiments on dogs subjected to local myocardial ischemia, we have shown a late and prolonged anti-ischemic and anti-arrhythmic effect of a single injection of the stable prostacyclin analogue, 7-oxo-PgI2. The protection was dependent on dose and time. Maximal effects were observed 48 hours after an optimal intramuscular dose of 50/micrograms/kg. To study the mechanism of this protective effect we have followed the time-dependent changes in transmembrane cation homeostasis induced by ischemia and reperfusion by measuring the intracellular potassium, sodium and calcium ion concentrations in Langendorff guinea pig heart preparations isolated from untreated control animals and from animals receiving a single intramuscular injection of 50/micrograms/kg 7-oxo-PgI2 48 hours before preparation. Global ischemia was produced by stopping perfusion for 25 minutes and was followed by reperfusion. In a second series, similarly treated and untreated hearts were fixed for electron microscopy after 25 minutes' global ischemia as well as after 15 minutes' reperfusion. Ischemia and reperfusion evoked a rapid loss of intracellular potassium and gain of sodium as well as an accumulation of calcium in the reperfusion phase. Pretreatment with 7-oxo-PgI2 prevented all these changes. It also prevented the shortening of the sarcomers and swelling of mitochondria induced by ischemia and the deposition of calcium-dense granules in mitochondria appearing after reperfusion. The findings support the hypothesis that 7-oxo-PgI2 has a delayed cytoprotective action which preserves normal transmembrane ion transport and normal structure of myocardial cells under conditions of ischemic and reperfusion injury.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardioscience 1 : 4 (1990), p. 279-286. -
További szerzők:Bálint Zsuzsa Karcsu Sarolta Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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6.

001-es BibID:BIBFORM041633
Első szerző:Szekeres László
Cím:Ion shifts in myocardial cells during ischemia and reperfusion and the effect of membrane stabilizing agents on ischemic ion transport / Szekeres L., Bálint Z., Tósaki A.
Dátum:1987
Megjegyzések:Ischemia-and reperfusion-induced time dependent changes of the intracellular K+/K+i/, Na+/Na+i/ and Ca2+/Ca2+i/ concentrations were analyzed in isolated Langendorff guinea pig hearts. In the ischemic period evoked by complete perfusion stop of 25 min duration a rapid loss of K+ and gain of Na+ was found. Ca2+i concentration started to increase only after 15 min of global ischemia. Reperfusion did not evoke substantial changes during the first minutes however Ca2+i very rapidly increased after 7 minutes of reperfusion. K+i rapidly increased above initial values in the first 3 minutes of reperfusion but then suddenly declined to the lowest ischemic level and remained at this level. Na+i concentration elevated by ischemia was not further affected by reperfusion. The membrane stabilizing antiarrhythmic agents: quinidine and lidocaine proved to be effective in preventing or moderating ischemia induced shifts in K+i and Na+i concentrations however did not affect Ca2+i content. This latter was markedly reduced by verapamil, a substance which failed to influence ischemic shifts of K+i and Na+i content.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biomedica Biochimica Acta. - 46 : 8-9 (1987), p. S527-S533. -
További szerzők:Bálint Zsuzsa Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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7.

001-es BibID:BIBFORM041649
035-os BibID:PMID:2557156
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Possible involvement of platelet activating factor in anaphylaxis of passively sensitised, isolated guinea pig hearts / Árpád Tósaki, Mátyás Koltai, Pierre Braquet, László Szekeres
Dátum:1989
ISSN:0008-6363
Megjegyzések: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.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Research. - 23 : 8 (1989), p. 715-22. -
További szerzők:Koltai Mátyás Braquet, Pierre Szekeres László
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8.

001-es BibID:BIBFORM041641
035-os BibID:PMID:3256423
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Pacing and reperfusion induced arrhythmias : protection by slow heart rate in the rat heart / Arpad Tosaki, Susan Balint, Laszlo Szekeres
Dátum:1988
ISSN:0008-6363
Megjegyzések:Using the isolated perfused rat heart with transient (10 min) regional ischaemia induced by coronary artery ligation, we have shown that slow heart rate can dramatically reduce the vulnerability of the myocardium to reperfusion induced ventricular fibrillation and ventricular tachycardia. In the heart rate range of 200-400 beats.min-1, slower heart rates exerted a frequency dependent protective effect against reperfusion induced arrhythmias. At the optimal rate of 200 beats.min-1, the incidence of total ventricular fibrillation (irreversible plus reversible) and ventricular tachycardia fell to 33% and 50% of their control values (100%). The anti-arrhythmic effect was achieved with only a minor (less than 20%) effect on coronary flow. To ascertain whether or not slow heart rate achieved an absolute reduction in vulnerability to arrhythmias irrespective of the duration of ischaemia, hearts were also subjected to 5, 10, 20, 30 or 40 min of ischaemia followed by 30 min of reperfusion with and without pacing at 200 beats.min-1. A bellshaped time-response profile was obtained in both groups. In unpaced controls (n = 12) this gave a maximal vulnerability to arrhythmias after 10 min of ischaemia. In the paced hearts (n = 12) the curve was shifted to the right, with a peak vulnerability at 20 min. These results show that the action of pacing is to exert a delaying effect which extends the duration of ischaemia that can be tolerated before the heart becomes vulnerable to reperfusion induced arrhythmias. Heart rate can have a substantial effect on reperfusion induced arrhythmias and should be considered when making therapeutic interventions and risk assessments in this setting.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cardiovascular Research. - 22 : 11 (1988), p. 818-825. -
További szerzők:Bálint Zsuzsa Szekeres László
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9.

001-es BibID:BIBFORM041639
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Diltiazem and the reduction of reperfusion-induced arrhythmias in the rat : protection is secondary to modification of ischemic injury and heart rate / Tosaki A., Szekeres L., Hearse D. J.
Dátum:1987
Megjegyzések:We have used the isolated rat heart with transient coronary artery occlusion to investigate whether diltiazem has an anti-arrhythmic action against reperfusion-induced ventricular arrhythmias. In the first series of studies (early administration group) the drug was administered 5 min prior to the induction of regional ischemia, this resulted in a dose-dependent reduction in reperfusion-induced ventricular fibrillation. With 5 X 10(-8), 10(-7), 5 X 10(-7), 10(-6) and 5 X 10(-6) mols of diltiazem/l, total ventricular fibrillation (reversible plus irreversible) was reduced from its control incidence of 100% (12/12) to 91%, 58% (P = less than 0.05), 17% (P = less than 0.001), 0% (P = less than 0.001) and 0% (P = less than 0.001) respectively. Heart rate was also reduced in a dose-dependent manner, falling from its control value of 268 +/- 6 beats/min to less than 50% with the highest concentration of diltiazem. Coronary flow was increased in a dose-dependent manner in the diltiazem treated groups. In additional studies with an anti-arrhythmic dose of diltiazem (5 X 10(-7) mols/l), hearts were paced to their drug free control value; under these conditions the anti-arrhythmic effect of diltiazem was lost. In further studies, diltiazem (10(-7) and 5 X 10(-7) mols/l) was administered just prior to reperfusion (late administration group), no anti-arrhythmic effects were observed. In additional studies we determined whether, with early administration, diltiazem (5 X 10(-7) mols/l) exerted its anti-arrhythmic effect by altering the relationship between the vulnerability to reperfusion-induced arrhythmias and the duration of preceding ischemia. In diltiazem-free control hearts a bell-shaped profile was observed with a maximum vulnerability after 10 min of ischemia (100% incidence of reperfusion-induced ventricular fibrillation). In diltiazem-treated hearts, a bell-shaped curve was also observed, however, its optimum was shifted to the right and downwards (20 min of ischemia gave maximum vulnerability [41%] to reperfusion-induced arrhythmias). We conclude that the ability of diltiazem to protect the isolated rat heart against reperfusion-induced arrhythmias is secondary to its anti-ischemic effect and in particular to its negative chronotropic properties.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 19 : 5 (1987), p. 441-451. -
További szerzők:Szekeres László Hearse, David J.
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10.

001-es BibID:BIBFORM041637
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Metoprolol reduces reperfusion-induced fibrillation in the isolated rat heart : protection is secondary to bradycardia / A. Tosaki, L. Szekeres, D. J. Hearse,
Dátum:1987
Megjegyzések:We studied the effect of metoprolol on the incidence of reperfusion-induced ventricular fibrillation in the isolated rat heart with transient coronary artery occlusion and reperfusion. When administered prior to ischemia, metoprolol produced a dose-dependent reduction in reperfusion-induced ventricular fibrillation. Thus, with 1, 10, 30, 50, 100, and 200 mumol/L metoprolol, total ventricular fibrillation (reversible plus irreversible) was reduced from its control incidence of 100% to 91%, 83%, 58% (p less than 0.05), 25% (p less than 0.001), 25% (p less than 0.001), and 0% (p less than 0.001), respectively. Heart rate was also reduced in a dose-dependent manner from its control value of 268 +/- 6 beats/min to less than 75% at the highest concentration of metoprolol. Coronary flow was unaffected by metoprolol. Doses of metoprolol (1 and 10 mumol/L) that had no significant effect on heart rate had no antiarrhythmic effect. In additional experiments with a higher dose of metoprolol (50 mumol/L), hearts were paced to the rate of the drug-free control group and the antiarrhythmic effect of metoprolol was lost. When drug-free control hearts had their heart rate reduced to that of the metoprolol-treated hearts, a similar antiarrhythmic effect was observed. When metoprolol was administered just prior to reperfusion, no antiarrhythmic effects were observed. In further studies, we investigated the effect of the early administration of metoprolol (50 mumol/L) on the relationship between the vulnerability to reperfusion-induced arrhythmias and the duration of preceding ischemia
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Cardiovascular Pharmacology. - 10 : 5 (1987), p. 489-497. -
További szerzők:Szekeres László Hearse, David J.
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11.

001-es BibID:BIBFORM041628
035-os BibID:PMID:4002266
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia / Árpád Tósaki, Mátyás Koltai, Ferenc Joó, Géza Adám, Péter Szerdahelyi, István Leprán, István Takáts, László Szekeres
Dátum:1985
ISSN:0039-2499
Megjegyzések:Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Stroke. - 16 : 3 (1985), p. 501-505. -
További szerzők:Koltai Mátyás Joó Ferenc (1949-) (vegyész) Ádám Géza Szerdahelyi Péter Leprán István Takáts István Szekeres László
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12.

001-es BibID:BIBFORM041625
035-os BibID:PMID: 2467078
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Protective effect of lidocaine against ischemia and reperfusion-induced arrhythmias and shifts of myocardial sodium, potassium, and calcium content / Arpad Tosaki, Susan Balint, Laszlo Szekeres
Dátum:1988
ISSN:0160-2446
Megjegyzések:Isolated guinea pig hearts subjected to global ischemia, were used to investigate whether lidocaine exerts an antiarrhythmic action against reperfusion-induced arrhythmias, and the effects of this drug upon myocardial ion contents during ischemia and reperfusion were studied. In the first series of experiments, the drug was administered 5 min prior to the induction of global ischemia and maintained during reperfusion. With 3.6 X 10(-6), 7.2 X 10(-6), 14.7 X 10(-6), and 29.5 X 10(-6) mol/L lidocaine, reperfusion-induced ventricular fibrillation and tachycardia were reduced from their control incidence of 83% and 100% to 41% and 58%, 33% (p less than 0.05) and 25% (p less than 0.001), 8% (p less than 0.01) and 8% (p less than 0.001), 0% (p less than 0.001) and 0% (p less than 0.001), respectively. The ion contents of myocardium were determined by atomic absorption spectrophotometer after washout of the ions from vasculature. Ischemia induced a marked accumulation of sodium and loss of potassium in the myocardial tissue. Both ischemia-induced sodium gain and potassium loss were significantly inhibited by lidocaine treatment. During reperfusion, sodium was further increased in the control group and this value was significantly lower in the lidocaine-treated group after 1 min of reperfusion. Sodium content remained at nearly constant level for the rest of reperfusion period. Potassium was suddenly increased during the first 5 min of reperfusion then continuously decreased until the end of reperfusion
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology. - 12 : 6 (1988), p. 621-628. -
További szerzők:Bálint Zsuzsa Szekeres László
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