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1.

001-es BibID:BIBFORM046506
Első szerző:Ferdinándy Péter
Cím:Loss of pacing-induced preconditioning in rat hearts : role of nitric oxide and cholesterol-enriched diet / Peter Ferdinandy, Zoltan Szilvassy, Laszlo I. Horvath, Tamas Csont, Csaba Csonka, Erzsebet Nagy, Reka Szentgyorgyi, Istvan Nagy, Matyas Koltai, Laszlo Dux
Dátum:1997
ISSN:0022-2828
Megjegyzések:We examined whether the inhibition ofnitric oxide (NO) synthesis by NG-nitro-L-arginine (LNNA) abolished pacing-induced preconditioning, and ifprolonged exposure to cholesterol-enriched diet led to the loss of preconditioning due to decreased cardiac NOformation. Therefore, Wistar rats fed 2% cholesterol-enriched diet or standard diet for 24 weeks were treatedwith a single dose of 1 mg/kg LNNA or its solvent at the end of the week 24, respectively. Isolated hearts fromall groups were subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats/min for 5 min, with 5-min interpacing periods, or time-matched non-preconditioning perfusion, followed by a10-min coronary occlusion, respectively. In the control group, coronary occlusion after a non-preconditioningprotocol decreased aortic flow (AF) from 45.4?2.4 to 15.6?1.5 ml/min, and resulted in a lactate dehydrogenase(LDH) release of 219?55 mU/min/g, however, preconditioning attenuated the consequences of coronary occlusion[AF: 27.3?1.7 ml/min (P<0.05); LDH: 44?14 mU/min/g (P<0.05)]. Preconditioning did not confer protectionin the LNNA-treated (AF: 17.4?1.5 ml/min; LDH: 151?21 mU/min/g), and/or in the high-cholesterol-fed groups(AF: 15.7?1.2 ml/min; LDH: 168?22 mU/min/g). Preconditioning was preserved however, when hearts weretreated with LNNA after the preconditioning protocol [AF: 29.6?2.2 ml/min (P<0.05); LDH: 48?17 mU/min/g (P<0.05)]. Both LNNA treatment and cholesterol-enriched diet markedly decreased cardiac NO content assayedby electron spin resonance spectroscopy. We conclude that NO may be involved in the triggering mechanism ofpacing-induced preconditioning, the protective effect of which is blocked by sustained exposure to dietarycholesterol, possibly by influencing cardiac metabolism of NO.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Pacing-induced
Nitric Oxide
NO
LNNA
Megjelenés:Journal of Molecular and Cellular Cardiology. - 29 : 12 (1997), p. 3321-3333. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Horváth László I. Csont Tamás Csonka Csaba Nagy Erzsébet (Szeged) Szentgyörgyi Réka Nagy István Koltai Mátyás Dux László
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2.

001-es BibID:BIBFORM046569
Első szerző:Ferdinándy Péter
Cím:Nitroglycerin-induced direct protection of the ischaemic myocardium in isolated working hearts of rats with vascular tolerance to nitroglycerin / P. Ferdinandy, Z. Szilvássy, T. Csont, C. Csonka, E. Nagy, M. Koltai, L. Dux
Dátum:1995
ISSN:0007-1188
Megjegyzések:We investigated whether nitroglycerin (NTG) was able to produce an anti-ischaemic effect in isolatedworking hearts of rats with vascular tolerance to NTG. Hearts isolated from tolerant and non-tolerantrats were subjected to 10 min coronary occlusion in the presence of 10r M NTG and/or its solvent. NTGalleviated ischaemia-induced deterioration of cardiac function and decreased lactate dehydrogenaserelease whilst having no effect on coronary flow nor the area of the ischaemic zone both in heartsisolated from NTG-tolerant and non-tolerant rats. The magnitude of the effect was similar in the twogroups. These results suggest that the anti-ischaemic effect of NTG involves direct myocardialmechanisms independent of its vascular action and that vascular tolerance to NTG does not affect thisdirect protective action.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Coronary occlusion
nitroglycerin
nitroglycerin tolerance
cardioprotection;
rat heart
Megjelenés:British Journal of Pharmacology. - 115 : 7 (1995), p. 1129-1131. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Csont Tamás Csonka Csaba Nagy Erzsébet (Szeged) Koltai Mátyás Dux László
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3.

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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4.

001-es BibID:BIBFORM046575
035-os BibID:PMID:1915586
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Effect of cicletanine on overpacing-induced ST-segment elevation in conscious rabbits : a comparison with verapamil / Zoltán Szilvássy, Mátyás Koltai, László Szekeres, Thierry Tarrade, Pierre Braquet
Dátum:1991
ISSN:0014-2999
Megjegyzések:We compared the effects of cicletanine (10 mg/kg i.v.) and verapamil (0.1 mg/kg i.v.) on heart rate, ventricular effective refractory period, systolic and diastolic arterial blood pressure and overpacing-induced ST-segment elevation detected by right ventricular intracavital electrogram in conscious rabbits. Cicletanine significantly reduced overpacing-induced ST-segment elevation, which is an indicator of myocardial ischemia and heart rate, but did not influence blood pressure and ventricular effective refractory period. Verapamil did not significantly influence ventricular effective refractory period, blood pressure or heart rate, but reduced the ST-segment elevation induced by frequency loading. These results suggest that acute treatment with cicletanine induces an anti-ischemic effect in the overpaced heart of conscious rabbits.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cicletanine
Verapamil
ST segment elevation
Frequency loading
Conscious rabbit
Megjelenés:European Journal of Pharmacology. - 199 : 3 (1991), p. 383-386. -
További szerzők:Koltai Mátyás Szekeres László Tarrade, Thierry Braquet, Pierre
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5.

001-es BibID:BIBFORM046510
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:The effect of continuous versus intermittent treatment with transdermal nitroglycerin on pacing-induced preconditioning in conscious rabbits / Z. Szilvassy, P. Ferdinandy, I. Nagy, I. Jakab, M. Koltai
Dátum:1997
ISSN:0007-1188
Megjegyzések:1 Tolerance to the hypotensive e?ect of nitroglycerin (NG) blocks preconditioning induced by rapidventricular pacing (RVP) in rabbits. In the present work the e?ect of continuous versus intermittenttreatment with transdermal nitroglycerin on the pacing-induced preconditioning phenomenon wasstudied in conscious rabbits.2 RVP (500 beats min71 over 5 min) increased left ventricular end-diastolic pressure (LVEDP) frombaseline 4.1+0.9 to postpacing 13.8+2.9 mmHg (P50.001) with a right intraventricular ST-segmentelevation of 1.25+0.13 mV, two indicators of myocardial ischaemia. These changes were signi?cantlyattenuated when the RVP period was preceded by a preconditioning pacing of the same rate andduration with an interpacing interval of 5 min.3 Protection by preconditioning was abolished when the animals had been made tolerant to thevasodilator e?ect of 30 mg kg71 NG by the application of transdermal NG (approx. 0.07 mg kg71 h71)over 7 days. Furthermore, transdermal NG per se attenuated both RVP-induced ST-segment elevationand LVEDP-increase over the 7 day period.4 With intermittent transdermal NG treatment (12 h 'patch on' vs 'patch o?'), neither development ofvascular tolerance nor attenuation of the NG- or preconditioning-induced anti-ischaemic e?ects wereobserved. However, the severity of pacing-induced myocardial ischaemia was signi?cantly increasedduring the 'patch o?' periods.5 In a second set of experiments, postpacing changes in cardiac cyclic GMP and cyclic AMP levelswere determined by means of radioimmunoassay in chronically instrumented anaesthetized open-chestrabbits with the same NG-treatment protocols. Preconditioning reduced postpacing increase in cyclicAMP with an increase in cyclic GMP concentrations in hearts of the untreated animals and in thosegiven patches intermittently during both 'patch on' and 'patch o?' periods. However, the preconditioninge?ect on either cyclic nucleotide was blocked in the tolerant animals.6 Transdermal NG increased resting levels of both cardiac cyclic nucleotides in the non-tolerant butnot in the tolerant state. The postpacing increase in cyclic AMP content was inhibited by transdermalNG, independent of vascular tolerance development, whereas, an increase in cyclic GMP content wasexclusively seen in the non-tolerant animals.7 We conclude that the anti-ischaemic effect of NG is independent of the cyclic GMP mechanism in thetolerant state. While intermittent NG therapy prevents development of vascular tolerance and preservespreconditioning, the nitrate-free periods yield an increased susceptibility of the heart to ischaemicchallenges.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Ischaemic preconditioning
nitrate tolerance
rapid pacing
cyclic GMP
intermittent nitrate therapy
Megjelenés:British Journal of Pharmacology. - 121 : 3 (1997), p. 491-496. -
További szerzők:Ferdinándy Péter Nagy I. Jakab Ildikó (farmakológus) Koltai Mátyás
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6.

001-es BibID:BIBFORM037828
035-os BibID:PMID:7952889
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Loss of preconditioning in rabbits with vascular tolerance to nitroglycerin / Z. Szilvassy, P. Ferdinandy, P. Bor, I. Jakab, J. Szilvassy, I. Nagy, J. Lonovics, M. Koltai
Dátum:1994
ISSN:0007-1188
Megjegyzések:A preceding right ventricular overdrive pacing (VOP) of 500 b.p.m. for 5 min, markedly reduced the severity of global myocardial ischaemia produced by a subsequent 5-min VOP in conscious rabbits. This VOP-induced preconditioning developed in parallel with an increase in cardiac cyclic guanosine 3':5'-monophosphate (cyclic GMP) content. VOP-induced preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of nitroglycerin (NG). In the heart of the NG-tolerant rabbits, neither VOP nor preconditioning increased cyclic GMP content. This suggests that changes by NG tolerance of cyclic GMP metabolism may account for the loss of VOP-induced preconditioning.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Ischaemic preconditioning
nitroglycerin tolerance
cyclic GMP
ST-segment elevation
LVEDP
rabbit heart
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 112 : 4 (1994), p. 999-1001. -
További szerzők:Ferdinándy Péter Bor P. Jakab Ildikó (farmakológus) Szilvássy Judit (1960-2022) (fül- orr- gégész) Nagy István Lonovics János (Szeged) Koltai Mátyás
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7.

001-es BibID:BIBFORM037829
035-os BibID:PMID:8825877
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:The loss of pacing-induced preconditioning in atherosclerotic rabbits : role of hypercholesterolaemia / Zoltan Szilvassy, Peter Ferdinandy, Judith Szilvassy, Istvan Nagy, Sarolta Karcsu, Janos Lonovics, Laszlo Dux, Matyas Koltai
Dátum:1995
ISSN:0022-2828
Megjegyzések:A brief rapid pacing has been shown to protect rabbit heart against global myocardial ischaemia induced by subsequent longer pacing. We studied whether pacing-induced preconditioning was reproducible in experimental hypercholesterolaemia. In conscious rabbits with an implanted right ventricular electrode and left ventricular polyethylene catheters, pacing of 500 bpm over 20 min induced an intracavitary ST-segment elevation of 3.2 +/- 0.41 mV, shortened ventricular effective refractory period and increased left ventricular end-diastolic pressure from prepacing 105 +/- 3.9 ms and 4.0 +/- 0.93 mmHg to post-pacing 62 +/- 6.4 ms and 27.9 +/- 7.2 mmHg, respectively. A 10-min preconditioning pacing followed by a 5-min interval markedly attenuated these test pacing-induced ischaemic changes. Rabbits were fed a cholesterol-enriched diet over 4, 8 and 12 weeks, responded to a 5- or 10-min pacing with ischaemic changes of the same degree as did controls to a 10- or 20-min pacing, respectively. A 4-week diet elevated total serum cholesterol from 1.7 +/- 0.4 to 24.1 +/- 2.9 mmol/l without apparent atherosclerotic lesions in the thoracic aorta assessed by Oil-Red O staining and planimetry, but it abolished protection induced by a 5-min preconditioning pacing. A 12-week diet increased serum cholesterol and lesion surface area to 26.9 +/- 3.2 mmol/l and 89.6 +/- 6.4%, respectively, and continued to block preconditioning. When these animals were refed normal chow over additional 6 weeks, serum cholesterol level dropped to 2.6 +/- 0.80 mmol/l with no change in atherosclerotic lesions, the preconditioning effect, however, recovered. We conclude that hypercholesterolaemia blocks preconditioning irrespective of the development of atherosclerosis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Ventricular overdrive pacing
Myocardial ischaemia
Preconditioning
Hypercholesterolaemia
Atherosclerosis
rabbit heart
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Molecular And Cellular Cardiology. - 27 : 12 (1995), p. 2559-2569. -
További szerzők:Ferdinándy Péter Szilvássy Judit (1960-2022) (fül- orr- gégész) Nagy István Karcsu Sarolta Lonovics János (Szeged) Dux László Koltai Mátyás
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