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1.

001-es BibID:BIBFORM086008
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Heme oxygenase related carbon monoxide and ventricular fibrillation / Istvan Bak, Gabor Papp, Ferenc Joo, Arpad Tosaki
Dátum:2002
ISSN:0022-2828
Tárgyszavak:Természettudományok Kémiai tudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Journal of Molecular and Cellular Cardiology. - 34 : 6 (2002), p. A6. -
További szerzők:Papp Gábor (1976-) (vegyész, kémikus) Joó Ferenc (1949-) (vegyész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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2.

001-es BibID:BIBFORM041699
Első szerző:Ferdinándy Péter
Cím:Pacing-induced Ventricular Fibrillation Leading to Oxygen Free Radical Formation in Aerobically Perfused Rat Hearts / Ferdinandy P., Das D. K., Tosaki A.
Dátum:1993
Megjegyzések:The objective of this study was to determine whether electrically-induced ventricular fibrillation can elicit oxygen free radical formation, even in the absence of ischemia and reperfusion. Rat hearts (n = 8 in each group) were perfused aerobically at 37 degrees C and ventricular fibrillation was induced by pacing (20 Hz, 1200 beats/min) for 10 min, during which time no changes in coronary flow rates were observed. In this study, electron spin resonance (ESR) studies using the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) demonstrated the formation of oxygen free radicals consisting of 1:2:2:1 quartet with peak concentration at the 3rd min of fibrillation in non-ischemic electrically fibrillating hearts. Since there were no significant changes in coronary flow rates during ventricular fibrillating (22.3 +/- 1.3 ml/min in control vs 22.3 +/- 0.9 ml/min in pacing-induced fibrillating group), the formation of oxygen free radicals could not be attributed to a pacing-induced ischemic event. In additional studies, hearts were paced by 10 Hz (600 beats/min), to demonstrate whether ventricular tachycardia could elicit free radical formation. In these experiments the genesis of oxygen free radicals was not observable after 1 min, 5 min, and 10 min of tachycardia, but a small amount of OH. radicals was detected at the 3rd min of ventricular tachycardia. When DMPO was infused into the heart giving a final perfusate concentration of 2.5 mmoles/litre during the pacing-induced fibrillation period, myocardial function (aortic flow, cardiac output, left ventricular developed pressure, first derivative of left ventricular developed pressure, and end-diastolic pressure) was significantly improved after the postfibrillating period. In conclusion, our studies clearly show that electrically-induced ventricular fibrillation is capable of eliciting free radical formation even in the absence of ischemia and reperfusion, and the cardioprotective effect of the spin trap is directly originated from its free radical trapping property and not from the other pharmacological activities of DMPO.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 25 : 6 (1993), p. 683-692. -
További szerzők:Das, Dipak Kumar Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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3.

001-es BibID:BIBFORM041643
035-os BibID:PMID:3398055
Első szerző:Hearse, David J.
Cím:Free radicals and calcium : simultaneous interacting triggers as determinants of vulnerability to reperfusion-induced arrhythmias in the rat heart / David J. Hearse, Arpad Tosaki
Dátum:1988
ISSN:0022-2828
Megjegyzések:Using the isolated perfused rat heart with regional ischemia and reperfusion, we have two antiarrhythmic interventions (the spin trap agent PBN [N-tert-butyl-alpha-phenylnitrone] and perfusate calcium reduction), administered just before reperfusion, to investigate mechanisms determining the vulnerability of the heart to reperfusion-induced ventricular fibrillation. Hearts were subjected to regional ischemia (5, 10, 20, 30 or 40 min) followed by reperfusion. Four groups were studied for each ischemic time: (i) control hearts with no antiarrhythmic intervention; (ii) hearts perfused with PBN (30 mumol/l) during the final 1 min of ischemia and throughout reperfusion, (iii) hearts perfused with low-calcium buffer (0.4 mmol/l) during the final 1 min of ischemia and throughout reperfusion and (iv) hearts perfused with PBN (30 mumol/l) and low-calcium (0.4 mmol/l) during the final 1 min of ischemia and throughout reperfusion. In control hearts, a bell-shaped time-vulnerability curve was obtained with 0, 91, 67, 33 and 17% of the hearts exhibiting irreversible fibrillation during reperfusion after 5, 10, 20, 30 and 40 min of ischemia, respectively. In the PBN group, the values were 8, 41 (P less than 0.05), 41, 33 and 8%, respectively. In the calcium reduction group the values were 17, 50, 8 (P less than 0.05), 8 and 0, respectively. Thus, PBN caused a significant reduction in reperfusion-induced ventricular fibrillation after 10 min of ischemia but had no significant effect with reperfusion after 20 min of ischemia. In contrast, calcium reduction had no significant effect after 10 min of ischemia but caused a significant reduction after 20 min of ischemia. When PBN treatment with calcium reduction were combined we obtained significant anti-arrhythmic effects after both 10 min (P less than 0.05) and 20 min (P less than 0.05) of ischemia. The additive effects of these two interventions, and the different ischemic-times after which they are most effective, has led us to propose that multiple triggers, each with different underlying mechanisms may be capable of initiating events which lead to ventricular fibrillation.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Molecular and Cellular Cardiology. - 20 : 3 (1988), p. 213-223. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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4.

001-es BibID:BIBFORM005161
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Overexpression of glutaredoxin-2 reduces myocardial cell death by preventing both apoptosis and necrosis / Norbert Nagy, Gautam Malik, Arpad Tosaki, Ye-Shih Ho, Nilanjana Maulik, Dipak K. Das
Dátum:2008
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 44 : 2 (2008), p. 252-260. -
További szerzők:Malik, Gautam Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Ho, Ye-Shih Maulik, Nilanjana Das, Dipak Kumar
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5.

001-es BibID:BIBFORM002214
035-os BibID:PMID:17397860
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Ischemic preconditioning involves dual cardio-protective axes with p38MAPK as upstream target / Norbert Nagy, Keisuke Shiroto, Gautam Malik, Chi-Kuang Huang, Mathias Gaestel, Maha Abdellatif, Arpad Tosaki, Nilanjana Maulik, Dipak K. Das
Dátum:2007
Megjegyzések:The existing literature indicates a crucial role of p38 MAP (mitogen-activated protein) kinase (p38MAPK) and its downstream target MAPKAP kinase 2 (MK2) in ischemic preconditioning (IPC). Accordingly, deletion of MK2 gene should abolish the cardioprotective ability of IPC. Interestingly, we were able to partially precondition the hearts from MK2(-/-) knockout mice suggesting the existence of an as yet unknown alternative downstream target of p38MAPK. A recent study from our laboratory also determined a crucial role of CREB (cyclic AMP response element binding protein) in IPC. Since CREB is a downstream target of MSK-1 (mitogen- and stress-activated protein kinase-1) situated at the crossroad of ERK (extracellular receptor kinase) and p38MAPK signaling pathways, we reasoned that MSK-1 could be a downstream molecular target for p38MAPK and ERK signaling in the IPC hearts. To test this hypothesis, the rat hearts were subjected to IPC by four cyclic episodes of 5 min ischemia and 10 min reperfusion. As expected, IPC induced the activation of ERK1/2, p38MAPK, MK2 and HSP (heat shock protein) 27 as evidenced by their increased phosphorylation; and the inhibition of p38MAPK with SB203580 almost completely, and the inhibition of ERK1/2 with PD098059 partially, abolished cardioprotective effects of IPC. Inhibition of MSK-1 with short hairpin RNA (shRNA) also abolished the IPC-induced cardioprotection. SB203580 partially blocked the effects of MSK-1 suggesting that MSK-1 sits downstream of p38MAPK. shRNA-MSK-1 blocked the contribution of both p38MAPK and ERK1/2 as it is uniquely situated at the downstream crossroad of both of these MAP kinases. Although MSK-1 sits downstream of both ERK1/2 and p38MAPK, ERK1/2 activation appears to play less significant role compared to p38MAPK, since its inhibition blocked MSK activation only partially. Consistent with these results, shRNA-MSK-1 blocked the partial PC in MK2(-/-) hearts, and in combination with SB203580, completely abolished the PC effects in the wild-type hearts. The IPC-induced survival signaling was almost completely inhibited with SB203580, and only partially with PD 098059 as evidenced from the inhibition patterns of IPC induced activation of CREB, Akt and Bcl-2. Again SB203580 alone or in combination with shRNA-MSK-1 inhibited IPC induced survival signal comparatively, suggesting that MSK-1 exists downstream of p38MAPK. Taken together, these results indicate for the first time MSK-1 as an alternative (other than MK2) downstream target for p38MAPK, which also transmits survival signal through the activation of CREB.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Molecular and Cellular Cardiology 42 : 5 (2007), p. 981-990. -
További szerzők:Shiroto, Keisuke Malik, Gautam Huang, Chi-Kuang Gaestel, Mathias Abdellatif, Maha Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Maulik, Nilanjana Das, Dipak Kumar
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6.

001-es BibID:BIBFORM041639
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Diltiazem and the reduction of reperfusion-induced arrhythmias in the rat : protection is secondary to modification of ischemic injury and heart rate / Tosaki A., Szekeres L., Hearse D. J.
Dátum:1987
Megjegyzések:We have used the isolated rat heart with transient coronary artery occlusion to investigate whether diltiazem has an anti-arrhythmic action against reperfusion-induced ventricular arrhythmias. In the first series of studies (early administration group) the drug was administered 5 min prior to the induction of regional ischemia, this resulted in a dose-dependent reduction in reperfusion-induced ventricular fibrillation. With 5 X 10(-8), 10(-7), 5 X 10(-7), 10(-6) and 5 X 10(-6) mols of diltiazem/l, total ventricular fibrillation (reversible plus irreversible) was reduced from its control incidence of 100% (12/12) to 91%, 58% (P = less than 0.05), 17% (P = less than 0.001), 0% (P = less than 0.001) and 0% (P = less than 0.001) respectively. Heart rate was also reduced in a dose-dependent manner, falling from its control value of 268 +/- 6 beats/min to less than 50% with the highest concentration of diltiazem. Coronary flow was increased in a dose-dependent manner in the diltiazem treated groups. In additional studies with an anti-arrhythmic dose of diltiazem (5 X 10(-7) mols/l), hearts were paced to their drug free control value; under these conditions the anti-arrhythmic effect of diltiazem was lost. In further studies, diltiazem (10(-7) and 5 X 10(-7) mols/l) was administered just prior to reperfusion (late administration group), no anti-arrhythmic effects were observed. In additional studies we determined whether, with early administration, diltiazem (5 X 10(-7) mols/l) exerted its anti-arrhythmic effect by altering the relationship between the vulnerability to reperfusion-induced arrhythmias and the duration of preceding ischemia. In diltiazem-free control hearts a bell-shaped profile was observed with a maximum vulnerability after 10 min of ischemia (100% incidence of reperfusion-induced ventricular fibrillation). In diltiazem-treated hearts, a bell-shaped curve was also observed, however, its optimum was shifted to the right and downwards (20 min of ischemia gave maximum vulnerability [41%] to reperfusion-induced arrhythmias). We conclude that the ability of diltiazem to protect the isolated rat heart against reperfusion-induced arrhythmias is secondary to its anti-ischemic effect and in particular to its negative chronotropic properties.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 19 : 5 (1987), p. 441-451. -
További szerzők:Szekeres László Hearse, David J.
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