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Your search keyword '"Ziegelhöffer, Attila"' showing total 141 results
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141 results on '"Ziegelhöffer, Attila"'

19. Effect of antihypertensive agents - captopril and nifedipine - on the functional properties of rat heart mitochondria.

Author

Kancirová, Ivana, Jašová, Magdaléna, Waczulíková, Iveta, Ravingerová, Táňa, Ziegelhöffer, Attila, and Ferko, Miroslav

Subjects
BIOENERGETICS, PHARMACOLOGY, MITOCHONDRIA, NIFEDIPINE, CAPTOPRIL
Abstract

Objective(s): Investigation of acute effect on cellular bioenergetics provides the opportunity to characterize the possible adverse effects of drugs more comprehensively. This study aimed to investigate the changes in biochemical and biophysical properties of heart mitochondria induced by captopril and nifedipine antihypertensive treatment. Materials and Methods: Male, 12-week-old Wistar rats in two experimental models (in vivo and in vitro) were used. In four groups, the effects of escalating doses of captopril, nifedipine and combination of captopril + nifedipine added to the incubation medium (in vitro) or administered per os to rat (in vivo) on mitochondrial ATP synthase activity and membrane fluidity were monitored. Results: In the in vitro model we observed a significant inhibitory effect of treatment on the ATP synthase activity (P<0.05) with nonsignificant differences in membrane fluidity. Decrease in the value of maximum reaction rate Vmax (P<0.05) without any change in the value of Michaelis- Menten constant Km, indicative of a noncompetitive inhibition, was presented. At the in vivo level, we did not demonstrate any significant changes in the ATP synthase activity and the membrane fluidity in rats receiving captopril, nifedipine, and combined therapy. Conclusion: In vitro kinetics study revealed that antihypertensive drugs (captopril and nifedipine) directly interact with mitochondrial ATP synthase. In vivo experiment did not prove any acute effect on myocardial bioenergetics and suggest that drugs do not enter cardiomyocyte and have no direct effect on mitochondria. [ABSTRACT FROM AUTHOR]

Published
2016

20. Calcium signaling-mediated endogenous protection of cell energetics in the acutely diabetic myocardiumThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research.

Author

Ziegelhöffer, Attila, primary, Waczulíková, Iveta, additional, Ferko, Miroslav, additional, Kincelová, Dana, additional, Ziegelhöffer, Barbara, additional, Ravingerová, Táňa, additional, Cagalinec, Michal, additional, Schönburg, Markus, additional, Ziegelhoeffer, Tibor, additional, Šikurová, Libuša, additional, Uličná, Oľga, additional, and Mujkošová, Jana, additional

Published
2009
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38. Suppression of reperfusion induced arrhythmias in the isolated rat heart: pretreatment with 7-oxo prostacyclin in vivo.

Author

Ravingerová, Tatiana, Tribulová, Narcisa, Ziegelhöffer, Attila, Styk, Jan, and Szekeres, Laszlo

Abstract

Objective: The aim was to investigate the late effect of pretreatment with 7-oxo prostacyclin on reperfusion induced arrhythmias in the isolated rat heart. Methods: Forty eight hours after intramuscular administration of drug in vivo (50 μg·kg−1 body weight), isolated Langendorff perfused rat hearts were subjected to 30 minutes of regional ischaemia and 5 minutes of reperfusion. Incidence and duration of ventricular arrhythmias in both pretreated and control groups were evaluated on reperfusion. Morphological examination was also performed. Results: In the untreated group reperfusion induced 75% of sustained ventricular fibrillation. Incidence of ventricular fibrillation, its duration, and arrhythmia score were significantly lower in the pretreated group. Pretreatment with 7-oxo prostacyclin had no effect on heart rate and coronary flow throughout the whole course of perfusion. Neither was the occluded zone size affected. Ultrastructure of ischaemic and reperfused myocardium was better preserved in the pretreated group. Conclusions: Antiarrhythmic action of 7-oxo prostacyclin was unrelated to changes in haemodynamics, thus suggesting the direct influence of the myocardium. The possible mechanism of action may involve maintenance of intracellular cation homeostasis (particularly of Na+ and Ca2+) due to a stimulation of sarcolemmal Na+ pump activity.Cardiovascular Research 1993;27:1051-1055 [ABSTRACT FROM PUBLISHER]

Published
1993

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