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1.

001-es BibID:BIBFORM041686
Első szerző:Abrahám Csongor
Cím:Adrenalectomy aggravates ischemic brain edema in female Sprague-Dawley rats with carotid arteries ligated / Cs. Abrahám, M. Koltai, F. Joó, Á. Tósaki, P. Szerdahelyi
Dátum:1992
ISSN:0079-6123
Megjegyzések:The effect of adrenalectomy has been investigated in a model of global cerebral ischemia. After bilateral carotid ligation the mortality rate was increased in adrenalectomized rats, and this effect was prevented by glucocorticoid pre-treatment. Adrenalectomy accelerated the appearance of the symptoms of cerebral ischemia, resulting in a moderate aggravation of brain edema and in a significant decrease in the concentration of high-energy phosphate esters. Our findings support the view that endogenous glucocorticoids may play a role in the amelioration of ischemic brain injuries in rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Progress in Brain Research. - 91 (1992), p. 23-27. -
További szerzők:Koltai Mátyás Joó F. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szerdahelyi Péter
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2.

001-es BibID:BIBFORM041706
035-os BibID:PMID:7698188
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Treatment with ranitidine of ischemic brain edema / Árpád Tósaki, Péter Szerdahelyi, Ferenc Joó
Dátum:1994
Megjegyzések:Cerebral ischemia was produced by bilateral common carotid artery occlusion in female Sprague-Dawley rats. Ranitidine, a histamine H2 receptor blocking agent, given intraperitoneally 30 min prior to ischemia, exerted a dose-dependent protective effect on water accumulation and ion shifts in the brain (Na+, K+ and Ca2+). To decide whether ranitidine can prevent ischemia-induced brain edema when given in the postischemic period, ranitidine (10 mg/kg i.p.) was administered 1, 2, and 3 h respectively after the onset of cerebral ischemia. Early (1 h) postocclusion treatment was still able to attenuate the ischemia-induced water accumulation and maldistribution of ions in the brain tissue.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Pharmacology. - 264 : 3 (1994), p. 455-458. -
További szerzők:Szerdahelyi Péter Joó Ferenc (1949-) (vegyész)
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3.

001-es BibID:BIBFORM041700
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of preconditioning on reperfusion arrhythmias, myocardial functions, formation of free radicals, and ion shifts in isolated ischemic/reperfused rat hearts / Tosaki A., Cordis G. A., Szerdahelyi P., Engelman R. M., Das D. K.
Dátum:1994
ISSN:0160-2446
Megjegyzések:The effects of preconditioning on development of reperfusion-induced ventricular fibrillation (VF), ventricular tachycardia (VT), free radical formation, and ion shifts, particularly those of Na, K, Ca, and Mg, were studied in isolated rat heart. Hearts were randomly divided into four groups: group I, aerobically perfused time-matched controls with no preconditioning or ischemia; group II, hearts subjected to 30-min global ischemia followed by 30-min reperfusion; group III, hearts subjected to one cycle of preconditioning, consisting of 5-min global ischemia plus 10-min reperfusion, followed by 30-min global ischemia plus 30-min reperfusion; and group IV, hearts subjected to four cycles of preconditioning (5-min ischemia plus 10-min reperfusion) followed by 30-min ischemia plus 30-min reperfusion. The incidences of VF and VT were reduced from their nonpreconditioned ischemic values of 100 and 100% in group II to 83 and 92% in group III and to 33% (p < 0.05) and 41% (p < 0.05) in group IV, respectively. Maximum malondialdehyde formation, as an indirect marker of free radicals, was observed after 30-min ischemia followed by 10-min reperfusion (0.72 +/- 0.1 nmol/ml) in the nonpreconditioned ischemic group (protocol II). One and four cycles of preconditioning reduced formation of malondialdehyde from the nonpreconditioned ischemic value of 0.72 +/- 0.1 to 0.35 +/- 0.02 and 0.26 +/- 0.02 nmol/ml (p < 0.05), respectively. The same trend was observed when free radical formation was directly detected by salicylic acid
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cardiovascular Pharmacology. - 23 : 3 (1994), p. 365-373. -
További szerzők:Cordis, Gerald A. Szerdahelyi Péter Engelman, Richard M. Das, Dipak Kumar
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4.

001-es BibID:BIBFORM041692
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of extracellular magnesium manipulation on reperfusion-induced arrhythmias and myocardial ion shifts in isolated ischemic reperfused rat hearts / Tosaki A., Szerdahelyi P., Engelman R. M., Das D. K.
Dátum:1993
ISSN:0022-3565
Megjegyzések:Isolated rat hearts were subjected to global ischemia followed by reperfusion, and a reduction in the incidence of reperfusion-induced ventricular fibrillation and ventricular tachycardia was brought about by increasing the extracellular Mg concentration in the perfusion buffer. Thus the incidence of ventricular fibrillation was reduced from its control value of 100% in 1.2 mM Mg to 83% by 2.4 mM Mg (P = N.S.), to 42% by 3.6 mM Mg (P < .05), to 17% by 4.8 mM Mg (P < .001) and to 17% by 9.6 mM Mg (P < .001). The corresponding values for ventricular tachycardia were 100% (control, 1.2 mM Mg) vs. 92% (P = N.S.), 50% (P < .05), 25% (P < .01) and 25% (P < .01), respectively. In further studies, extracellular Ca was reduced by 50% (1.2 mM) in the perfusion buffer just before ischemia and during reperfusion. The incidence of ventricular fibrillation was reduced from its control value of 83% in 1.2 mM Mg to 75% by 1.8 mM Mg (P = N.S.), to 33% by 2.4 mM Mg (P < .05), to 17% by 3.6 mM Mg (P < .01) and to 8% by 4.8 mM Mg (P < .01). The incidence of ventricular tachycardia followed the same pattern. Myocardial Na, K, Ca and Mg were measured by atomic absorption spectrophotometer after the removal of ions from the extracellular space. In controls, 30 min of ischemia resulted in 3- and 4-fold accumulation of myocardial Na and Ca, respectively, and during reperfusion these values were similar to the values for 30-min ischemia.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Pharmacology And Experimental Therapeutics. - 267 : 3 (1993), p. 1045-1053. -
További szerzők:Szerdahelyi Péter Engelman, Richard M. Das, Dipak Kumar
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5.

001-es BibID:BIBFORM041691
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Potassium channel openers and blockers : do they possess proarrhythmic or antiarrhythmic activity in ischemic and reperfused rat hearts? / Tosaki A., Szerdahelyi P., Engelman R. M., Das D. K.
Dátum:1993
ISSN:0022-3565
Megjegyzések:Cromakalim is a member of the new antihypertensive drug family possessing an action that involves an increased K efflux in vascular and cardiac muscle. We studied the contribution of opening of ATP-sensitive K channel to the development of reperfusion-induced arrhythmias and myocardial ion shifts, particularly that of Na, K, Ca and Mg in isolated rat hearts. After 30 min of global ischemia, cromakalim (1 to 30 microM) failed to reduce reperfusion arrhythmias. On the postischemic-reperfused myocardium in a subset of hearts unresponsive to reperfusion-induced arrhythmias (duration of ischemia was reduced to 25 min), cromakalim treatment was associated with a higher incidence of reperfusion ventricular fibrillation (VF) and ventricular tachycardia (VT) as compared to the controls (100% VF and 100% VT in treated vs. 41% VF and 50% VT in controls, P < .05). Proarrhythmic effects of cromakalim were also reflected in a maldistribution of myocardial ions. At concentrations of 3, 10 and 30 microM of glibenclamide, a K channel blocker, a significant reduction in the incidence of reperfusion-induced VF and VT was observed, and an attenuation in the maldistribution of myocardial ion contents induced by ischemia/reperfusion was found. The reduction in myocardial contractility was detected at relatively high concentrations (10 and 30 microM) in both cromakalim- and glibenclamide-treated groups. The proarrhythmic effect of cromakalim (30 microM) was abolished by 3 microM of glibenclamide, suggesting that the increased tendency to develop reperfusion arrhythmias is associated with the cromakalim-induced K efflux.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Pharmacology And Experimental Therapeutics. - 267 : 3 (1993), p. 1355-1362. -
További szerzők:Szerdahelyi Péter Engelman, Richard M. Das, Dipak Kumar
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6.

001-es BibID:BIBFORM041689
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Reperfusion-induced arrhythmias and myocardial ion shifts : a pharmacologic interaction between pinacidil and cicletanine in isolated rat hearts / Tosaki A., Szerdahelyi P., Das D. K.
Dátum:1992
Megjegyzések:Pinacidil is a member of the new antihypertensive drug family possessing an action that involves an increased potassium efflux in vascular and cardiac muscle. We investigated the contribution of opening of ATP-sensitive potassium channel to the development of reperfusion-induced arrhythmias and myocardial ion shifts, particularly that of Na+, K+, Ca2+, and Mg2+ in isolated rat hearts. After 30 min of normothermic global ischemia, pinacidil with 1 to 60 mumol/l failed to reduce the incidence of reperfusion-induced arrhythmias, even on the postischemic/reperfused myocardium in a subset of hearts unresponsive to reperfusion-induced arrhythmias (the duration of ischemia was reduced to 25 min), pinacidil treatment was associated with a greater incidence of reperfusion-induced arrhythmias (100%) as compared to the control value (50%). These proarrhythmic effects of pinacidil were also reflected in a maldistribution of myocardial ion contents both in nonischemic and ischemic/reperfused hearts. Cicletanine, a furopyridine antihypertensive agent that has no effect on coronary resistance, reduced the incidence of reperfusion arrhythmias, and its antiarrhythmic effect was antagonized by pinacidil. The same observation was made in relation to myocardial ion content, e.g., pinacidil-induced K+ loss and Ca2+ gain were antagonized by cicletanine, both in nonischemic and ischemic/reperfused hearts. It is hypothesized that the increased tendency to develop reperfusion-induced ventricular fibrillation is associated with the pinacidil-induced K+ efflux. The present study does not attempt to address the question of specific ionic currents; however, it has been suggested that proarrhythmic and antiarrhythmic effects of pinacidil and cicletanine, respectively, may relate to same receptor sites in which the latter may reflect a specific blockade of the outward K+ ion current via ATP-sensitive K+ channels. If this is so, the use of K+ channel openers as antihypertensive agents may be of particular concern in that population of postinfarction patients who are known to be at high risk of sudden coronary death.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Basic Research in Cardiology. - 82 : 4 (1992), p. 366-384. -
További szerzők:Szerdahelyi Péter Das, Dipak Kumar
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7.

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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