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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:BIBFORM046643
035-os BibID:PMID:2674453
Első szerző:Szekeres László
Cím:7-oxo-PgI2 induced late appearing and long-lasting electrophysiological changes in the heart in situ of the rabbit, guinea-pig, dog and cat / L. Szekeres, Z. Szilvassy, Éva Udvary, Ágnes Végh
Dátum:1989
ISSN:0022-2828
Megjegyzések:We have previously observed a long-lasting antiischemic and anti-arrhythmic effect induced by prostacyclin (PgI2) or its stable analogue, 7-oxo-PgI2-ephedrine salt in dogs subject to local myocardial ischemia. This protection appeared when the vasodilating and platelet aggregation inhibiting effect of PgI2 or its analogue was over and persisted even 72 h after treatment. We have also found that short incubation with 7-oxo-PgI2 may induce a long-lasting prolongation of the action potential duration and of the effective refractory period in the isolated rabbit papillary muscle preparation without affecting the membrane potential or the rate of rise of the action potential.Our present experiments have shown a 7-oxo-PgI2 induced, dose-dependent prolongation of the ventricular functional refractory period in conscious rabbits and anesthetized dogs, as well as an increase of the QT interval in the ECG in both species and also in conscious guinea-pigs. In all three species 50 ?g/kg i.m. dose proved to be optimal, evoking maximal effect 48 h after treatment. In conscious rabbits this pre-treatment prevented the train of non-stimulated extra beats induced by premature stimuli. Furthermore it also prevented widening of the QRS complex appearing in non-treated controls after programmed stimulation. Pre-treatment significantly increased electrical fibrillo-flutter thresholds in the auricles and ventricles of anesthetized cats. These electrophysiological changes seem to be closely related to the 7-oxo-PgI2 induced, late appearing and long-lasting protection from ischemic and reperfusion arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
7-oxo-PgI2
Action potential duration
Functional refractory period
Fibrillo-flutter threshold
Megjelenés:Journal of Molecular and Cellular Cardiology. - 21 : 6 (1989), p. 545-554. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Udvary Éva Végh Ágnes
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DOI
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3.

001-es BibID:BIBFORM046509
035-os BibID:PMID:9236151
Első szerző:Szekeres László
Cím:Delayed cardiac protection against harmful consequences of stress can be induced in experimental atherosclerosis in rabbits / Laszlo Szekeres, Zoltan Szilvassy, Peter Ferdinandy, Istvan Nagy, Sarolta Karcsu, Sándor Csáti
Dátum:1997
ISSN:0022-2828
Megjegyzések:Multiple brief periods of rapid ventricular pacing confer bothshort- and long-term protection on the ischaemic heart. The duration of the short-term protection does notexceed 2 h, whereas the long-term protective effect appears several hours after the inducing insults, with maximalprotection 24?48 h later. Up to now, delayed cardiac protection by preceding ischaemic insults against harmfulconsequences of stress has been produced in the normal, healthy animal only. The purpose of this study was,therefore, to test whether delayed cardiac protection can be induced in experimental atherosclerosis in rabbitsproduced by feeding cholesterol-rich diet over 2 months. Repeated brief periods of rapid ventricular pacing wereused to induce delayed protection of the heart. Moderation of post-pacing right intracavitary ST segment elevationand that of the left ventricular end-diastolic pressure (both produced by ventricular overpacing: 500 beats/minfor 15 min) were found in normal animals as well as in those fed cholesterol-enriched diet. The short-livedprotection induced by a single 'preconditioning' pacing was reproducible only in normal animals. As measuredby means of radioimmunoassay, the protective effect of either short- or long-term protection appeared inparallel with an attenuation of ischaemia-induced increase in cardiac cyclic AMP content, in both normal andatherosclerotic rabbits. An increase in cardiac cyclic GMP content was characteristic of the short- but not longtermprotection. These results suggest that the delayed cardiac protection by preceding multiple brief rapidpacings operates even in experimental atherosclerosis, but the short-term protection induced by a singlepreconditioning stimulus is lost.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Atherosclerosis
ischaemia
Megjelenés:Journal of Molecular and Cellular Cardiology. - 29 :7 (1997), p. 1977-1983. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Ferdinándy Péter Nagy István Karcsu Sarolta Csáti Sándor
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4.

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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