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1.

001-es BibID:BIBFORM020469
Első szerző:Csont Tamás
Cím:Direct myocardial anti-ischaemic effect of GTN in both nitrate-tolerant and nontolerant rats : a cyclic GMP-independent activation of KATP / Tamás Csont, Zoltán Szilvássy, Ferenc Fülöp, Saviana Nedeianu, Tibor Páli, Árpád Tósaki, László Dux, Péter Ferdinandy
Dátum:1999
ISSN:0007-1188
Megjegyzések:Abstract1. We have recently demonstrated that glyceryl trinitrate (GTN) exerts a direct myocardial anti-ischaemic effect in both GTN-tolerant and nontolerant rats. Here we examined if this effect is mediated by GTN-derived nitric oxide (NO) and involves guanosine 3'5' cyclic monophosphate (cyclic GMP) and ATP-sensitive K+ channels (KATP). 2. Rats were treated with 100 mg kg-1 GTN or vehicle s.c. three times a day for 3 days to induce vascular GTN-tolerance or nontolerance. Isolated working hearts obtained from either GTN-tolerant or nontolerant rats were subjected to 10 min coronary occlusion in the presence of 10-7 M GTN or its solvent. 3. GTN improved myocardial function and reduced lactate dehydrogenase (LDH) release during coronary occlusion in both GTN-tolerant and nontolerant hearts. 4. Cardiac NO content significantly increased after GTN administration in both GTN-tolerant and nontolerant hearts as assessed by electron spin resonance. However, cardiac cyclic GMP content measured by radioimmunoassay was not changed by GTN administration. 5. When hearts from both GTN-tolerant and nontolerant rats were subjected to coronary occlusion in the presence of the KATP-blocker glibenclamide (10-7 M), the drug itself did not affect myocardial function and LDH release, however, it abolished the anti-ischaemic effect of GTN. 6. We conclude that GTN opens KATP via a cyclic GMP-independent mechanism, thereby leading to an anti-ischaemic effect in the heart in both GTN-tolerant and nontolerant rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Direct myocardial
anti-ischaemic effect
Direct myocardial anti-ischaemic effect
effect of GTN
GTN
cyclic activation of K(ATP)
cyclic GMP-independent activation of K(ATP)
K(ATP)
Megjelenés:British Journal of Pharmacology 128 : 7 (1999), p. 1427-1434. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Fülöp Ferenc (Szeged) Nedeianu, Saviana Páli Tibor Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Dux László Ferdinándy Péter
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2.

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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3.

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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4.

001-es BibID:BIBFORM020561
Első szerző:Ferdinándy Péter
Cím:Rapid pacing-induced preconditioning is recaptured by farnesol treatment in hearts of cholesterol-fed rats : role of polyprenyl derivatives and nitric oxide / Peter Ferdinandy, Csaba Csonka, Tamás Csont, Zoltán Szilvássy, László Dux
Dátum:1998
Megjegyzések:AbstractWe have previously shown that hypercholesterolemia leads to the loss of pacing-induced preconditioning (PC), possibly due to the impairment of cardiac nitric oxide (NO) synthesis. It has been shown that excess exogenous cholesterol inhibits formation of several polyprenyl derivatives involved in signal transduction. In the present study, we examined whether PC and cardiac NO synthesis are restored by treatment with the key polyprenyl product, farnesol, in cholesterol-fed rats. Rats fed 2% cholesterol-enriched/control diet for 24 weeks were given i.p. 5 microM/kg farnesol/vehicle, respectively. An hour later, hearts were isolated and prepared for 'working' perfusion, then subjected to PC/non-PC protocols of 3 intermittent periods of pacing of 5 min duration at 10 Hz, followed by a 10 min coronary occlusion to test the effect of PC. PC increased ischemic aortic flow (AF) from its control value of 15.6+/-1.5 to 27.3+/-1.7 mL/min (p < 0.05). PC was not observed in hearts obtained from hypercholesterolemic rats (AF: 15.7+/-1.2 mL/min), however, it reappeared in the farnesol-treated hypercholesterolemic group (AF: 31.8+/-3.4 mL/ min, p < 0.05). In tissue samples from the left ventricle, cholesterol-diet markedly decreased the intensity of the electron spin resonance spectra of NO obtained after in vivo spin trapping with Fe2+-diethyl-dithio-carbamate complex. Farnesol-treatment did not influence cardiac NO content in the cholesterol-fed or in the control group. These results show that the lost PC can be recaptured by farnesol-treatment in hypercholesterolemia, however, farnesol-treatment does not restore cardiac NO synthesis.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Rapid pacing-induced
farnesol treatment
cholesterol-fed
polyprenyl derivatives
nitric oxide
Megjelenés:Molecular and Cellular Biochemistry. - 186 : 1-2 (1998), p. 27-34. -
További szerzők:Csonka Csaba Csont Tamás Dux László Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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5.

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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