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1.

001-es BibID:BIBFORM041657
Első szerző:Blasig, Ingolf E.
Cím:Inverse relationship between ESR spin trapping of oxyradicals and degree of functional recovery during myocardial reperfusion in isolated working rat heart / Blasig I. E., Ebert B., Hennig C., Pali T., Tosaki A.
Dátum:1990
Megjegyzések:STUDY OBJECTIVE: The aim of the study was to investigate the generation of free oxyradicals as factors in myocardial ischaemia-reperfusion pathology. DESIGN: Isolated perfused rat hearts were subjected to 30 min global ischaemia followed by reperfusion. The spin trap 5,5-dimethyl-1-pyrroline-1-oxide was added to the effluent of the heart to avoid pharmacological interaction with the heart. The effluent was then analysed by electron spin resonance spectroscopy. MATERIALS: Studies were performed on hearts of 51 male Sprague-Dawley rats, weight 300-350 g. MEASUREMENTS AND RESULTS: During reperfusion, the formation of hydroxyl radical adducts of the trap was observed, with a maximal value after 3 min. The initial amount of radicals trapped during the first 3 min of reperfusion showed an inverse correlation with the degree of heart function restored within 30 min of reperfusion. Spearman's rank correlation coefficients were calculated to be -0.734 for heart rate, -0.825 for left ventricular developed pressure, -0.787 for the maximum of its first derivative, -0.787 for coronary flow, and -0.796 for aortic flow (p less than 0.05, n = 10, in each instance). No statistically significant correlation was found between the cumulative amount of radicals trapped in the effluent during the initial phase of reperfusion and the duration of ventricular fibrillation, duration of ventricular tachycardia, or number of ventricular ectopic beats (registered during 30 min reperfusion). CONCLUSIONS: The application of spin trapping to the effluent of isolated perfused hearts allows the generation of oxyradicals to be characterised without interaction of the trap with the heart. It also allows the time course of radical production to be investigated, and can detect relative changes in their intensity. These are important factors in the study of the pathogenic role of free radicals generated during reperfusion of an ischaemic heart.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardioscular Research. - 24 : 4 (1990), p. 263-270. -
További szerzők:Ebert, Berndt Hennig, Christian Pali Tibor Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM041684
Első szerző:Koltai Mátyás
Cím:Effect of BN 50739, a new platelet activating factor antagonist, on ischaemia induced ventricular arrhythmias in isolated working rat hearts / Koltai M., Tosaki A., Hosford D., Esanu A., Braquet P.
Dátum:1991
ISSN:0008-6363
Megjegyzések:STUDY OBJECTIVE: The aim was to investigate the role of platelet activating factor (PAF) in myocardial ischaemia by using BN 50739, a new specific PAF receptor antagonist with a hetrazepine framework. DESIGN: Isolated working rat hearts were subjected to regional ischaemia, induced by ligation of the left main coronary artery for 30 min, followed by reperfusion. BN 50739 was applied at concentrations of 10(-7), 10(-6), 10(-5) and 5 X 10(-5) M, and its effects on the incidence of ischaemia induced and reperfusion induced ventricular tachycardia and ventricular fibrillation and heart functions, such as heart rate, coronary flow, aortic flow, left ventricular developed pressure (LVDP), its first derivative (LVdP/dtmax), and left ventricular end diastolic pressure (LVEDP), were determined. EXPERIMENTAL MATERIAL: Studies were performed on isolated working hearts of male Sprague-Dawley rats weighing 300-360 g. Hearts were perfused with BN 50739 dissolved in dimethylsulphoxide. Control hearts were perfused with the vehicle. MEASUREMENTS AND MAIN RESULTS: Regional ischaemia triggered ventricular arrhythmias showing high incidence between 12 and 20 min with peak appearance at 16 min. BN 50739 induced dose dependent protection against ventricular tachycardia and fibrillation: incidences declined from their respective control values of 91% and 75% to 33% (p less than 0.05) and 8% (p less than 0.05) after exposure to 10(-5) M, and to 25% (p less than 0.05) and 8% (p less than 0.05) after exposure to 5 X 10(-5) M concentrations. Reperfusion of the ischaemic myocardium resulted in an immediate appearance of ventricular tachycardia and fibrillation, but these were not suppressed by the PAF antagonist. Regional ischaemia slightly reduced heart rate, markedly decreased coronary flow, aortic flow, LVDP and LVdP/dtmax, and increased LVEDP. With the exception of LVEDP, these variables were not influenced by the drug. BN 50739, applied at a concentration of 5 X 10(-5) M, reduced LVEDP significantly during the whole ischaemic period. CONCLUSIONS: Under in vitro conditions PAF is likely to be involved in the genesis of ischaemia induced ventricular arrhythmias since BN 50739, a specific PAF receptor antagonist, exerts a protective effect against these rhythm disturbances. This suggests that PAF antagonists may have benefit in the clinical management of acute myocardial ischaemia.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research. - 25 : 5 (1991), p. 391-397. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Hosford, David Esanu, Andre Braquet, Pierre
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041703
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Reperfusion induced arrhythmias are caused by generation of free radicals / Tosaki A., Das D. K.
Dátum:1994
ISSN:0008-6363
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
note
Megjelenés:Cardiovascular Research. - 28 : 3 (1994), p. 422. -
További szerzők:Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM041650
035-os BibID:PMID:2620326
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of low extracellular sodium concentration on reperfusion induced arrhythmias : changes in the myocardial sodium, potassium and calcium contents in isolated guinea pig hearts / Árpád Tósaki, Mátyás Koltai, Pierre Braquet
Dátum:1989
ISSN:0008-6363
Megjegyzések: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.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Research. - 23 : 12 (1989), p. 993-1000. -
További szerzők:Koltai Mátyás Braquet, Pierre
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM041156
035-os BibID:PMID:8689644
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:The evolution of diabetic response to ischemia/reperfusion and preconditioning in isolated working rat hearts / Árpád Tosaki, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1996
ISSN:0008-6363
Megjegyzések:OBJECTIVE: Studies have shown that the diabetic heart exhibits abnormalities in cellular ion transport, which can affect susceptibility to reperfusion-induced ventricular fibrillation (VF), tachycardia (VT) and functional derangements. It has been shown that "preconditioning" renders the heart very resistant to a subsequent prolonged ischemic episode. This phenomenon has been extensively studied in healthy myocardium, but such a study has not been previously done in diseased (hypertrophic or myopathic) hearts. METHODS: We studied the incidence of reperfusion-induced VF, VT, cardiac function, and ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia/reperfusion in isolated hearts from rats with streptozotocin-induced diabetes. Following 2, 4, 6, and 8 weeks of diabetes, hearts were isolated and subjected to 30 min global ischemia followed by reperfusion. RESULTS: In the 2-week diabetic group the total incidence of VF and VT was reduced from their non-diabetic age-matched control value of 100 and 100% to 42 (P < 0.05) and 42% (P < 0.05), respectively. Such a reduction in the incidence of VF and VT was not observed with progressive diabetes (4, 6, and 8 weeks). In the 2-week diabetics, the reduction in the VF and VT was reflected in the improvement of postischemic function, the reduction of ischemia and reperfusion-induced Na+ and Ca2+ gains, and the prevention in K+ and Mg2+ loss. This diabetes-induced initial protection was not seen in the 4- and 6-week diabetics, and a deterioration of postischemic function was observed in the 8-week diabetics. Four cycles of preconditioning, each consisting of 5 min ischemia followed by 10 min reperfusion, failed to reduce the incidence of VF and VT, improve cardiac function, and prevent ion shifts induced by 30 min ischemia followed by 30 min reperfusion in 4- and 8-week diabetics. CONCLUSIONS: In the early phase of diabetes the heart is more resistant to ischemia/reperfusion than the non-diabetic heart. Preconditioning does not afford protection against a prolonged period of ischemia in diabetics, indicating that preconditioning may be a "healthy heart phenomenon".
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Research. - 31 : 4 (1996), p. 526-536. -
További szerzők:Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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