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001-es BibID:	BIBFORM046511
035-os BibID:	PMID:8595627
Első szerző:	Ferdinándy Péter
Cím:	KATP channel modulation in working rat hearts with coronary occlusion: effects of cromakalim, cicletanine, and glibenclamide / Péter Ferdinandy, Zoltán Szilvassy, Marie T. Droy-Lefaix, Thierry Tarrade, Matyas Koltai
Dátum:	1995
ISSN:	0008-6363
Megjegyzések:	OBJECTIVES: We studied the effects of ATP-sensitive potassium channel (KATP) modulation on ischemic cardiac performance and reperfusion-induced ventricular fibrillation (VF), and assessed the contribution of KATP to the cardioprotective and anti-arrhythmic effect of the anti-hypertensive drug cicletanine. METHODS: Isolated working rat hearts, subjected to a 10-min coronary occlusion followed by reperfusion, were perfused in the presence of vehicle, 0.1-60 microM cromakalim, an opener of KATP; 3-60 microM cicletanine; and 0.1-10 microM glibenclamide, a blocker of KATP, respectively. RESULTS: All concentrations of cicletanine, similarly to 0.1-10 microM cromakalim, attenuated ischemia-induced deterioration of aortic flow, left ventricular developed pressure, and left ventricular end-diastolic pressure. In contrast to cromakalim, cicletanine did not increase coronary flow. Cicletanine (60 microM) and cromakalim (10 and 60 microM) significantly reduced the incidence of reperfusion-induced VF; however, 60 microM cromakalim triggered VF during ischemia. Lower concentrations of cromakalim and cicletanine did not produce an anti-arrhythmic effect. Cardiac functional parameters were concentration dependently worsened by glibenclamide, and the drug did not change the incidence of VF. Glibenclamide (0.1 microM) did not significantly affect cardiac performance, but it did abolish the anti-ischemic effect of cromakalim (1-10 microM) and cicletanine (60 microM). Glibenclamide suppressed the anti-arrhythmic effect of 10 and 60 microM cromakalim; however, it did not affect the anti-arrhythmic effect of cicletanine. CONCLUSIONS: (i) The anti-ischemic but not the anti-arrhythmic effect of cicletanine may involve opening of KATP. (ii) opening of KATP attenuates, inhibition of the channel exacerbates functional consequences of coronary occlusion, and (iii) KATP opening attenuates reperfusion-induced VF, but it triggers ischemia-induced VF. KATP blocking does not affect VF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban cicletanine myocardial ischemia myocardial function arrhythmias reperfusion potassium channel openers sulphonylureas
Megjelenés:	Cardiovascular Research. - 30 : 5 (1995), p. 781-787. -
További szerzők:	Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Droy-Lefaix, Marie-Thérèse Tarrade, Thierry Koltai Mátyás
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001-es BibID:	BIBFORM046573
035-os BibID:	PMID:832479
Első szerző:	Szekeres László
Cím:	Moderate stress by cardiac pacing may induce both short term and long term cardioprotection / László Szekeres, Julius Gy. Papp, Zoltán Szilvassy, Éva Udvary, Ágnes Vegh
Dátum:	1993
ISSN:	0008-6363
Megjegyzések:	Objective: The aim was to investigate whether moderate ischaemic stress induced by brief periods of cardiac pacing to twice the normal heart rate protects the heart from the electrophysiological and haemodynamic consequences of subsequent periods of rapid pacing. Methods: Conscious rabbits with implanted right ventricular electrodes and a permanent catheter in the left ventricular cavity were studied. Hearts were paced at a rate of 500?min?1 for 5 min. The resulting transient ST segment elevation in the intracavital electrogram, the ventricular effective refractory period, and the left ventricular end diastolic pressure were measured. Results: After discontinuation of pacing, a shortlasting ST segment elevation appeared in the endocardial electrogram, together with a transient rise in left ventricular end diastolic pressure. These changes were significantly reduced after a second pacing, provided that this was applied not later than 30 min after the first pacing; maximum protection occurred when there was a 5 min interval between these pacing periods. Serial stimulation (10 pacing periods with a 5 min interval between each) gave a similar protection to that resulting from a single pacing period. The protection was lost after 1 h; however, 24 h and 48 h (but not 72 h) after the end of serial stimulation there was again a reduction in postpacing ST segment and left ventricular end diastolic pressure elevation. At these times the ventricular effective refractory period was prolonged. The cyclo-oxygenase inhibitor sodium meclofenamate (1-2 mg?kg?1) prevented the early protection. Conclusions: The results suggest that brief periods of rapid pacing induce both short term and long term cardioprotection, as shown by reduced electrophysiological and haemodynamic consequences of subsequent pacing periods. Endogenous prostanoids might play a role in the short term cardioprotection.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban ventricular overpacing ischemia short term cardioprotection long term cardioprotection
Megjelenés:	Cardiovascular Research. - 27 : 4 (1993), p. 593-596. -
További szerzők:	Papp Gy. Julius (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Udvary Éva Végh Ágnes
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