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001-es BibID:	BIBFORM027563
Első szerző:	Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:	Non-specific caspase inhibition reduces infarct size and improves post-ischaemic recovery in isolated ischaemic/reperfused rat hearts / Peter Kovacs, Istvan Bak, Levente Szendrei, Miklos Vecsernyes, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:	2001
Megjegyzések:	Myocardial ischaemia and reperfusion lead to myocardial cell death due, at least in part, to apoptotic mechanisms. Although cysteinyl aspartate-specific proteinase (caspase) activation is a major event and the most-cited culprit in the development of apoptosis, its potential contribution to ischaemic myocardial cell death is largely unknown. To study the role of caspase activation, isolated rat hearts (n=6 per group) were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion. A non-selective [0.1 or 0.5 microM acetyl-Tyr-Val-Ala-Asp chloromethylketone (YVAD-cmk)] or selective caspase inhibitors [0.07 or 0.2 microM acetyl-Asp-Glu-Val-Asp-cmk (Ac-DEVD-cmk, caspase-3 inhibitor); 0.07 or 0.2 microM benzoxycarbonyl-Leu-Glu-OMe-His-Asp(OMe)-fluoromethylketone (z-LEHD-fmk, caspase-9 inhibitor)] were added to the perfusate at the start of reperfusion. Non-selective caspase inhibition with 0.1 or 0.5 microM YVAD-cmk limited infarct size: (21 +/- 4%, P<0.05; 17 +/- 3%, P<0.05, respectively) compared with the ischaemic/reperfused control (32 +/- 5%). In hearts treated with 0.1 or 0.5 microM caspase II non-selective inhibitor, the fraction of terminal-deoxynucleotidyl-transferase deoxyuridine nick end labelling (TUNEL)-positive myocyte nuclei in the infarcted zone was reduced from the ischaemic/reperfused non-treated control of 11.2 +/- 2.1% to 6.2 +/- 1.6% (P<0.05) and 1.2 +/- 0.2% (P<0.05), respectively. The recovery of post-ischaemic cardiac function (coronary flow, aortic flow and left-ventricular developed pressure) improved significantly with the application of the non-selective caspase inhibitor as well. In hearts perfused with specific caspase inhibitors (caspase-3 and caspase-9) there was no significant reduction in the infarct size, no improvement in post-ischaemic cardiac function and no reduction of apoptotic cell death. We conclude that non-specific inhibition of caspases may be therapeutically beneficial in myocardial ischaemia/reperfusion-induced damage, while selective caspase inhibitors may fail to prevent such reperfusion-induced injury in our model system.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Naunyn-Schmiedeberg's archives of pharmacology 364 : 6 (2001), p. 501-507. -
További szerzők:	Bak István (1975-) (vegyész, analitikus, farmakológus) Szendrei Levente Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM027561
Első szerző:	Pataki Tünde (farmakológus, klinikai farmakológus)
Cím:	Regulation of ventricular fibrillation by heme oxygenase in ischemic/reperfused hearts / Tunde Pataki, Istvan Bak, Csaba Csonka, Peter Kovacs, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:	2001
Megjegyzések:	We have assessed the relationship between reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO) mRNA expression using northern blotting, reverse transcription-polymerase chain reaction (RT-PCR), and enzyme activity in isolated working ischemic/reperfused rat hearts. Isolated hearts were subjected to 30 min of global ischemia followed by 120 min of reperfusion. Upon reperfusion with VF, cardiac function was registered (n = 6 in each group), and HO mRNAs and enzyme activities were measured at the end of reperfusion in hearts that showed VF or did not develop VF. The expression of HO-1 mRNA (about fourfold) was observed in ischemic/reperfused nonfibrillated myocardium in comparison with the nonischemic control hearts. In those hearts when VF was developed, the expression of HO-1 mRNA was not observed in comparison with the nonischemic control myocardium. The results measured by RT-PCR and enzyme analysis support the data obtained by northern blotting. In additional studies, we decided to approach the question from a different angle. Thus, the purpose of our work was also to study the role of HO expression and enzyme activity in electrically fibrillated hearts without the ischemic/reperfused protocol. To simulate the period of 10 min of reperfusion-induced VF, hearts were electrically fibrillated, then defibrillated, and perfused for an additional 110 min, and HO-1 mRNA expression and enzyme activities were determined. Thus, electrically induced VF resulted in about 60%, 60%, and 70% reduction in HO-1 mRNA expression, RT-PCR signal intensity, and enzyme activity, respectively, compared with the nonfibrillated ischemic/reperfused group. In conclusion, our data provide evidence that the development of reperfusion-induced VF inhibits HO-1 mRNA expression and enzyme activity in both electrically fibrillated myocardium and ischemic/reperfused fibrillated hearts. The results clearly show that HO-1 mRNA expression and enzyme activity were increased in ischemic/reperfused nonfibrillated myocardium, suggesting that interventions that are able to increase HO-1 mRNA expression and enzyme activity may prevent the development of VF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Antioxidants & redox signaling 3 : 1 (2001), p. 125-134. -
További szerzők:	Bak István (1975-) (vegyész, analitikus, farmakológus) Csonka Csaba Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM027560
Első szerző:	Pataki Tünde (farmakológus, klinikai farmakológus)
Cím:	Grape seed proanthocyanidins improved cardiac recovery during reperfusion after ischemia in isolated rat hearts / Tunde Pataki, Istvan Bak, Peter Kovacs, Debasis Bagchi, Dipak K. Das, Arpad Tosaki
Dátum:	2002
ISSN:	0002-9165
Megjegyzések:	Background: Increasing evidence shows that red wine consumption has cardioprotective effects. These effects have been attributed to the polyphenolic compounds in grapes. Objective: We studied the effects of red grape seed proanthocyanidins on the recovery of postischemic function in isolated rat hearts. Design: Two groups of rats were fed different doses of proanthocyanidin-rich extract for 3 wk and another group was untreated and served as controls. The animals were then anesthetized and the hearts were isolated and subjected to 30 min of ischemia followed by 2 h of reperfusion. Coronary effluents were collected during the third minute of reperfusion for measurement of oxygen free radicals by using electron spin resonance spectroscopy. Results: In rats treated with 50 and 100 mg grape seed proanthocyanidins/kg, the incidence of reperfusion-induced ventricular fibrillation was reduced from its control value of 92% to 42% and 25%, respectively (P < 0.05 for both). The incidence of ventricular tachycardia showed the same pattern. In rats treated with 100 mg proanthocyanidins/kg, the recovery of coronary flow, aortic flow, and developed pressure after 60 min of reperfusion was improved by 32% ± 8%, 98% ± 8%, and 37% ± 3%, respectively (P < 0.05 for all) compared with untreated control rats. Electron spin resonance studies indicated that proanthocyanidins significantly inhibited the formation of oxygen free radicals. In rats treated with 100 mg proanthocyanidins/kg, free radical intensity was reduced by 75% ± 7% (P < 0.05) compared with the control rats. Conclusion: Grape seed proanthocyanidins have cardioprotective effects against reperfusion-induced injury via their ability to reduce or remove, directly or indirectly, free radicals in myocardium that is reperfused after ischemia.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	American Journal Of Clinical Nutrition 75 : 5 (2002), p. 894-899. -
További szerzők:	Bak István (1975-) (vegyész, analitikus, farmakológus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Bagchi, Debasis Das, Dipak Kumar Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat Szerző által megadott URL
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