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001-es BibID:	BIBFORM042021
Első szerző:	Ferdinándy Péter
Cím:	Cicletanine improves myocardial function deteriorated by ischemia/reperfusion in isolated working rat hearts / Ferdinandy Péter, Koltai Mátyás, Tósaki Árpád, Berthet Philippe, Tarrade Thierry, Esanu André, Braquet Pierre
Dátum:	1992
Megjegyzések:	The effect of cicletanine, a novel furopyridine antihypertensive drug was compared with that of nitrendipine, a dihydropyridine slow calcium channel blocker, on cardiac function and reperfusion-induced ventricular arrhythmias in isolated working rat hearts subjected to 10-min ischemia induced by ligation of the left main coronary artery followed by 10-min reperfusion. Before ischemia, cicletanine and nitrendipine, perfused at concentrations of 3 x 10(-5), 6 x 10(-5), 10(-4), and 2 x 10(-4) or 10(-8) M, respectively, did not influence heart rate (HR), LV developed pressure (LVDP), its first derivative (LVdP/dtmax), and LV end-diastolic pressure (LVEDP), whereas aortic flow (AF) was decreased by 2 x 10(-4) M cicletanine only. Coronary flow (CF) remained unchanged by various cicletanine concentrations but was slightly increased by nitrendipine. In the concentration range of 3 x 10(-5)-10(-4) M, cicletanine improved AF either in ischemia or during reperfusion, whereas 2 x 10(-4) M had no such effect. Nitrendipine slightly attenuated ischemia/reperfusion-induced decrease in AF. Cicletanine and nitrendipine enhanced LVDP during ischemia. Ischemia-induced deterioration of LVdP/dtmax was reduced by cicletanine, during reperfusion, but this parameter was reduced by nitrendipine and the highest cicletanine concentration. Cicletanine decreased LVEDP significantly during ischemia and reperfusion, but nitrendipine had no such effect. All cicletanine concentrations reduced the incidence of irreversible ventricular fibrillation (VF) during reperfusion, an effect roughly concentration dependent in the range of 3 x 10(-5)-10(-4) M, whereas nitrendipine had no influence on arrhythmias.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban MSH
Megjelenés:	Journal of Cardiovascular Pharmacology. - 19 : 2 (1992), p. 181-189. -
További szerzők:	Koltai Mátyás Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Berthet, Philippe Tarrade, Thierry Esanu, Andre Braquet, Pierre
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM041688
Első szerző:	Koltai Mátyás
Cím:	Effect of cicletanine on reperfusion-induced arrhythmias and myocardial ion contents : a comparison with furosemid / Koltai M., Tosaki A., Berthet P., Tarrade T., Esanu A., Braquet P.
Dátum:	1992
Megjegyzések:	We studied the effects of cicletanine, a furopyridine antihypertensive drug, and furosemide, a loop diuretic, on ventricular arrhythmias, such as sustained ventricular fibrillation (VF) and ventricular tachycardia (VT), and myocardial ion content in Langendorff rat hearts subjected to 30 min global ischaemia then 10 min reperfusion. Myocardial Na+, K+, Ca2+ and Mg2+ concentrations were measured by washout technique and atomic absorption spectrophotometry before and after ischaemia and reperfusion. Drugs were either perfused (acute treatment) or orally gavaged daily to the rats for 14 days before isolation of their hearts (chronic treatment). Under in vitro conditions 10(-5), 3 x 10(-5), 10(-4) or 3 x 10(-4) M of cicletanine reduced the incidence of sustained VF and VT from the control values of 91% and 100% to 83% and 100%, 50% (P less than 0.05) and 67%, 33% (P less than 0.01) and 50% (P less than 0.05), 25% (P less than 0.01) and 41% (P less than 0.05), respectively. Chronic treatment with 3, 10, 30 or 100 mg.kg-1.day-1 of cicletanine also resulted in a dose-dependent anti-arrhythmic effect. Neither acute (10(-5), 3 x 10(-5) and 10(-4) M) nor chronic furosemide treatment (3, 10 and 30 mg.kg-1.day-1) influenced the incidence of arrhythmias. Acute treatment with cicletanine or furosemide did not change myocardial ion concentrations, in non-ischaemic hearts, while chronic treatment with 30 mg.kg-1.day-1 furosemide significantly reduced myocardial Na+, K+ and Mg2+ content and increased Ca2+ concentration. Both acute and chronic cicletanine treatments attenuated ischaemia/reperfusion-induced myocardial Na+ and Ca2+ gains and K+ loss, while furosemide did not
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	European Heart Journal. - 13 : 3 (1992), p. 395-403. -
További szerzők:	Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Berthet, P. Tarrade, T. Esanu, Andre Braquet, Pierre
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM041685
Első szerző:	Koltai Mátyás
Cím:	Cicletanine : a novel approach to cardioprotection in spontaneously hypertensive rats / Matyas Koltai, Arpad Tosaki, Thierry Tarrade, Philippe Berthet, Andre Esanu, Pierre G. Braquet
Dátum:	1991
ISSN:	0954-6928
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Coronary Artery Disease. - 2 (1991), p. 941-944. -
További szerzők:	Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Tarrade, Thierry Berthet, Philippe Esanu, Andre Braquet, Pierre
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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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 DOI
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